Talk:Mitochondrion/Archive prior talk

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This is an ARCHIVE talk-page for article: Mitochondrion.

Main talk-page: Talk:Mitochondrion


Topics from 2002-2004[edit]

Endosymbiotic theory[edit]

More information about mitochondiral DNA and endosymbiosis theory is needed here! Some is available at -[ at 12:13, 14 August 2002]

Different page[edit]

This should rather go to endosymbiotic hypothesis or a new page, I guess.

Aragorn2 15:25, 16 Sep 2003 (UTC)

non-photosynthetic eukaryotes[edit]

can you give an example of one without mitochondria? I'm skeptical.168... 08:14, 11 Jan 2004 (UTC) Never mind. I found the Diplomonadida.168... 08:18, 11 Jan 2004 (UTC)

mtDNA recombination possible in humans[edit]

Hopefully it has been noticed that Kreytsberg et al. have released a shocking paper. Although it doesn't directly refute the use of mtDNA as a marker in population genetics, it casts doubt on this method.

I have changed the article to reflect this. I refer to ' Kraytsberg et al., Recombination of Human Mitochondrial DNA, Science 2004 304: 981'.

Topics from 2005[edit]

Interesting theory or established fact?[edit]

I can't recall where but I seem to remember hearing that mitochondria may have been one of the first lifeforms in the primeval sea and started out as an independent lifeform which may later on have struck up some kind of mutually beneficial relationsship with another lifeform thus becoming the foundation of all life that it is today. Was that just nonsense? If not I think it deserves some mention because it is frightfully interesting isn't it? Preisler 21:19, 25 Apr 2005 (UTC)

Ah it's already mentioned I see.. The bio lingo in the first couple of paragraphs made me skip it.. This article really is a bit hard to read for the layman..
That's a side effect of the fact that this article is mostly edited by people specifically interested in cell biology, whch tends to be individuals involved in the field, or at least studying it at the university level. Without looking again at the article myself, may I ask which parts you found the most difficult? – ClockworkSoul 18:42, 4 December 2005 (UTC)

Author Help[edit]

Who are the authors that wrote this article? How should I cite this article for my report? I need help in this area. Mitochondria are so interesting! For those who haven't, I suggest you read A Wind in The Door by Madeline L'Engle- it's an amazing fictional/factual story on mitochondria suggesting that farandolae might exist on mitochondria.

There are numerous contributors—from the article page, click the "history" tab to see all the people who have worked on this article. To see how to cite the article, please click on the "cite this article" link in the toolbox to the left of the article. Hope this helps! — Knowledge Seeker 18:34, 4 December 2005 (UTC)
Of course, it bears repeating that encyclopedia (and especially Wikipedia) articles should generally not be used as sources except in a very general way. Albatrossish 05:19, 18 March 2006 (UTC)
Yeah, I read A Wind in the Door. It's a great book. I'm planning to write some more for this article, about recent studies. By the way, do you think someone should add a section to this article called "Mitochondia in Fiction?"

Topics from 2006[edit]

Dropped paragraph[edit]

There is a paragraph in Use in population genetic studies section in rev.38776689 which somehow got dropped when reverting vanadalism. It may contain relevant information but I cannot judge. The paragraph reads: Recent studies have, however, cast doubt on this hypothesis. Kraytsberg et al. showed that mitochondrial recombination is possible in humans (Science 304:981, May 2004, pubmed #15143273).

image for mitochondrion (light microscope)[edit]

I've taken the liberty of removing the Image:Mitochondria in cell.jpg from the top in support of the comment from Rob at the top of the talk page. Though I am not familiar with light microscopy of mitochondria, I have several electron microscopy images in my 'molecular biology of the cell', and they all show structures much more resembling the diagram, and certainly without any threadlike structures. The light microscopy image does not add much information and perhaps even adds some confusion. Jens Nielsen 10:53, 10 February 2006 (UTC)

has my support Adenosine | Talk 09:08, 12 February 2006 (UTC)

Percentage of cytosol or cytoplasm?[edit]

Re "[mitochonria] can occupy up to 25% of the cell's cytosol". Since the cytosol is the portion of the cytoplasm without the organelles, logically mitochonria cannot "occupy" any part of the cytosol. A-giau 06:35, 14 February 2006 (UTC)

Well seen. I've changed it accordingly (don't hesitate to do so yourself if you spot such mistakes - just add explanation).
A related point: Can anyone confirm the 25% figure? A citation would be good to have. Jens Nielsen 21:18, 14 February 2006 (UTC)

Revised: Comment on Images in Mitochondrion Entry[edit]

The previous light microscopic image of a mitochondrial reticulum in a cell that was removed in February should be restored. Mitochondria are a dynamic reticulum in most cells, with long and short cylinders fissioning and fusing to form an elaborate branched network. The football shape in textbooks is a throwback to a time before three dimensional confocal fluorescence and electron tomographic imaging. It is also biased by results with isolated mitochondria, which do tend to be more round.

The current cartoon is also inaccurate in the representation of cristae as random infoldings. They are invaginations that originate at tubular openings into the boundary or peripheral region of the inner membrane. I have uploaded a model (MitoModelCAM.jpg) based on electron tomography that shows this. (I'd be happy to work with whoever drew the cartoon to help make it more accurate. I think a simple fix is possible.) You can also click on the website links (on the top page of the mitochondrion entry) for the national microscopy centers in Albany NY and San Diego CA that have been generating 3D images of mitochondria for over 10 years.

(I hold the copyright to the uploaded image and hereby release it into the public domain.)

Carmmann 19:38, 5 March 2006 (UTC)

I would suggest 2 images be used in this article - one simplified one (such as the current one) which shows clearly the main structure, plus another which is more accurate in a real situation. --Scohoust 14:23, 18 March 2006 (UTC)

I entered the room here to try and get the idea, and the image, out there, that the mitochondria are a network. Carmmann has said it pretty eloquently. Mitochondria comprise a network of tunnelling electronic devices in every cell; and there are numerous images of selectively stained mitochondria that show this physical networking in vivo in situ quite clearly. What we've got in the Wiki article, that Carmmann refers to as "the football shape", and as a "cartoon", is really a problem, IMHO. This image of isolated footballs keeps us from figuring out how they form an electronic network.Richard8081 19:45, 3 July 2007 (UTC)

Where are the images CarmMann says were uploaded MitoModelCAM.jpg ???Richard8081 19:47, 3 July 2007 (UTC)
Here is the image (Image:MitochondrionCAM.jpg) as well as the associated reference (PMID 16054341) authored by Carmmann. David D. (Talk) 20:44, 3 July 2007 (UTC)
Richard, what do you mean by "tunnelling electronic devices"? David D. (Talk) 20:33, 3 July 2007 (UTC)

For reference, the other image in question is Image:Mitochondria in cell.jpg. (It doesn't seem to me to illustrate a reticulum all that well, though.) For a quick overview of mitochondrial reticula you might want to see Intro of this paper. -R. S. Shaw 22:11, 3 July 2007 (UTC)

David -- the is a full text paper with all the illustrations included. The one illustration of green-fluorescent protein labelled mitochondria in yeast says it all. thanks. I remember seeing that picture a while ago, never could find it again. The first time I saw a picture like that, the authors said "Yeast have one large mitochondrion ..." Never forgot that. The wiki article needs an illustration of this genre. There are numerous illustrations of selectively stained HeLa cells that are striking in their ramification of the mito network. Amazing images, when one considers that the competition is the football from the textbook.

the article itself (EMBO Rep. 2002 June 17; 3(6): 527–531. doi: 10.1093/embo-reports/kvf113. Copyright © 2002 European Molecular Biology Organization Reviews Merging mitochondria matters Cellular role and molecular machinery of mitochondrial fusion Benedikt Westermann) includes the following paragraph, relevant to mitochondria being networked electronic devices:

"The establishment and maintenance of an intracellular mitochondrial continuum by continuous membrane fusion and fission events bears relevance for the dissipation of energy in the cell. Experiments with human fibroblasts using fluorescent labeling techniques proved that the mitochondrial membrane potential (Δψ) is equal over the whole length of a mitochondrion. This was demonstrated by damaging the mitochondrial membranes locally by irradiation with a laser beam, which led to an immediate collapse of Δψ in an extended network of interconnected filaments (Amchenkova et al., 1988). This suggests that mitochondrial filaments represent electrically united systems that facilitate the delivery of energy to remote parts of the cell (Skulachev, 2001). In muscle cells, for example, a multilayer of mitochondria is found below the outer cell membrane (sarcolemma) where the oxygen supply is high. These organelles are connected by mitochondrial filaments to mitochondria located in the oxygen-poor core part of the muscle fiber. It has been proposed that the mitochondrial network in muscle cells serves to transmit the membrane potential generated by subsarcolemmal mitochondria to intermyofibrillar organelles, which can then use oxygen from the cell periphery to produce ATP in the core of the muscle fiber (Skulachev, 2001). Morphological observations (Bakeeva et al., 1983) are in agreement with the view that mitochondrial fusion is required for the establishment of the intermyofibrillar network and maintenance of muscle function."

I quoted the whole paragraph; it's out of context enough without chopping it up. Note the phrase "electrically united systems". Funny, I didn't have such an elegant paragraph in mind when I wrote my original comment, that mitochondria are a network of electronic devices. Thus do we learn. Thanks for the reference. (I haven't actually finished reading it; it is seriously about fission/fusion of membranes, the mechanics of which I probably won't remember for long).

Now, about the "tunnelling" in my statement that mitochondria in cells are a network of tunnelling electronic devices. A few weeks ago (May 2007) I paid a visit to Dr Britton Chance in Philadelphia (I worked for him years ago), for the express purpose of asking him one question: "Dr Chance, are mitochondria electronic devices?" and he replied, all 95 years of him, "Tunnelling electronic devices." I looked up tunnelling afterward, and I think I know why he said that, but I am not the guy to go to, to delineate it further. If he says that electron transport is electron tunnelling, okay by me. My kid is an EE senior at MIT, maybe I'll ask him to educate me further about it; unfortunately he's only a CS whiz, so I won't find out much, I reckon. I'll go see what Wikipedia has to say about electron tunnelling. Richard8081 01:23, 4 July 2007 (UTC) I thought about it some more and wrote down my thoughts at Richard8081 03:11, 8 July 2007 (UTC)

Use in Population Genetic Studies[edit]

Quoth the article, "Because of the unique matrilineal transmission of mitochondrial DNA, scientists in population genetics and evolutionary biology often use data from mitochondrial DNA sequences to draw conclusions." Scientists use data to draw conclusions?? Shocking! I am not knowledgeable enough to expand this into a more informative sentence. Albatrossish 05:22, 18 March 2006 (UTC)

[citation needed][edit]

Why do you doubt this statement? If it didn't undergo destruction soon after fertilization then mitochondiral inheritence *wouldn't* be matrilineal. pschemp | talk 04:13, 13 July 2006 (UTC)

For reference, the article sentence I tagged with {fact} was:
"However, the mitochondria provided by the sperm are targeted for destruction very soon after entry into the egg."
I would like a source for this because there are many other possible mechanisms which could cause matrilineal inheritance of mitochondrial genes. Just offhand I can come up with these alternatives:
  • the paternal mitochondria aren't transferred into the egg by the sperm or aren't permitted to enter by the egg.
  • only the nucleus enters the egg
  • all entering material is transferred to the egg's nucleus, where the paternal mitochondria cannot reproduce
  • the paternal mitochondria in the cytosol are not permitted to reproduce by some mechanism, thus being diluted into essential nonexistence eventually
Given that there are many possible ways to explain matrilineal inheritance, it seems like the article should support the particular assertion it makes. Whatsmore, the particular mechanism of targetting is of interest. -R. S. Shaw 05:02, 13 July 2006 (UTC)
The original statement was correct, and I replaced it with the correct source reference. (It had been replaced by a mistake with a general textbook cited -- not good.) 08:41, 16 July 2006 (UTC)
That's not a mistake, that was a correct, sourced statement from a college level textbook. If you can prove it is wrong, please do, but you'll have to find a source. Don't arbitrarily remove things like that if you don't know what you are doing please. pschemp | talk 15:05, 16 July 2006 (UTC)
So, then, why did you replace a statement supported by a peer-reviewed journal source along with commentary in Science News with a general textbook source? "we do not delete SOURCED material"? Unless they disagree with our preconceptions? TempAcctPubTerm 22:44, 16 July 2006 (UTC)
There is no need for using such inflammatory terms as "flat out wrong". Also, it is customary to discuss such removals on the the talk page first, in a civil manner. Had you done this, much conflict could have been avoided. pschemp | talk 01:19, 17 July 2006 (UTC)

Need a microscope picture at top[edit]

Since the duplicate diagram was removed, it would be good to have a microphotograph up at the top of the article next to the intro. I recommend this one. It is free because it is a product of a US government agency. Its caption is: Electron micrograph of a single mitochondrion showing the organized arrangement of the protein matrix and the inner mitochondrial membranes. (Photo: U.S. Dept. of Health and Human Services/National Institutes of Health)[1]

I would upload it but the silly public terminal I'm on will not let me save images to disk. 06:58, 16 July 2006 (UTC)

I uploaded it for you. Here is the image: Image:Mitochondrion 186.jpg. Its a little small but better than nothing. David D. (Talk) 07:07, 16 July 2006 (UTC)
Thanks! 08:41, 16 July 2006 (UTC)

Eloping mitochondrion[edit]

I remember when I were younger, we learned that since the mitochondria has it's own set of DNA, it could easily escape. I remember talking to my teacher a lot about this, but haven't really found anything in those words exactly about it! Was he just pulling my leg, or is this a possibility, if so, should it be included in the article, or is it too un-scientific? (talk)

Pulling your leg. A good bit of the original DNA a mitochondria had has been transferred to the nucleus of eukaryotic cells, therefore, it doesn't have everything it needs to survive outside the cell. pschemp | talk 15:07, 16 July 2006 (UTC)
yes, but it could still "escape" (if you can follow) and the consequences I believe would be fatal. Or maybe I'm trying to say, there is nothing that really constitutes the mitochondria to stay, they just choose to! (erh... this might seem naïve, it was just a childhood fascination that I suddenly remembered) 15:24, 16 July 2006 (UTC)
No, it can't escape. They don't choose to be there, because they can't "choose" to do anything. In fact, the cytoskeleton holds them in place somewhat. Like I said before, mitochondria do not have the nesseccary DNA to live outside the cell, or to "choose" anything. They are completely dependent on the cell, and the cell on them. I think you may be thinking about Endosymbiotic theory which may explain their original configuration as free bacteria, but the mitochondria around today have changed too much to be able to "choose" to leave the cell. Also see the fiction section of this article, there was a sci-fi book written about mitochondria that revolt, perhaps you are mixing fact with fiction. pschemp | talk 18:37, 16 July 2006 (UTC)
I talked to a friend last night that told me she also have heard of this. They discussed it in her cell biology class, in theory it could happen her teacher said! Of course this was a while ago, and I'm sure there are a lot of theories on the subject, but they learned that the mitochondria once was a Microorganism that the human cell accepted. And no, I weren't referring to the Parasite Eve series, but thanks for taking the time to reply! 14:56, 17 July 2006 (UTC)

confusing sentence[edit]

Can anybody explain this to me, please:

The uniparental inheritance of mitochondria is thought to result in intragenomic conflict, such as seen in the petite mutant mitochondria of some yeast species. It is possible that the evolution of separate male and female sexes is a mechanism to resolve this organelle conflict.

How's the petite mitochondria a sign of intragenomic conflict? And how would sexuality resolve the conflict? --euyyn 03:10, 20 November 2006 (UTC)

I have read in many books about this (e.g. Dawkins). I'll dig out more references later. These sentences are talking about heterosexual reproduction. Imagine a species which reproduces via single-sex mechanism (two eggs merge with two eggs). This must have been how sexual reproduction started in the first place. Now, the eggs need a mechanism to propel them in the world and to maintain cell operations, so they can find their mates. And possibly mitochondria were the energy sources. Once two eggs merge, their regular genes recombine, but the mitochonrion organelles do not recombine. So different mitochondria of different lineage from two parents will live side by side in the same offspring cells. Now, from a mitochondrion's selfish perspective, it will fare better and reproduce more offsprings of its own, if it manages to kill mitochondria from the other parent. Over time, they will evolve the ability to do just that, and in fact, we observe this in a lot of creatures. This results in unnecessary casualties, yielding bad reproduction rates statistically. In animals with heterosexual reproduction, the sperm becomes so small that it does not contain a lot of mitochondria. And the few that it contains get quickly killed off by those from the egg, once the sperm gets into the egg. Heterosexual reproduction is thus a genetically stable strategy. Fred Hsu 04:13, 20 November 2006 (UTC)

Thank you for answering. Let's see if I understood it... eh, so some mithocondrion in a female once muted in a way that made it kill sperm mithocondria, so it had double offsprings than usual, and so it scattered by Darwin. Right? Well but that would be a natural adaptation of the mithocondria to heterosexuality, not the mithocondria causing heterosexuality... what am I missing? --euyyn 23:00, 24 November 2006 (UTC)

I think the theory runs like this: if a species does not have distinct (ie ova/sperm) gametes, then the conflict of mitochondria encourages development of sperm gametes differentiated from ova gametes. If two equivalent gametes fuse as part of sexual reproduction, then the mitochondria will develop factors which attack and kill (or sterilize) any "different" mitochondria they encounter. That means when the equivalent gametes fuse, the mitochondira will kill each other until only a few (all of one type) are left, leaving the cell with too few mitochondria. Hence the nuclear genome develops ways of suppressing the mitochondira from one of the two gametes, thus leading to the development of ova differentiated from sperm. -R. S. Shaw 03:27, 25 November 2006 (UTC)
Thank you. That's a much better and more concise explanation. Fred Hsu 15:18, 25 November 2006 (UTC)

I almost forgot that I promised to find references. This is mentioned in many books, but the one I particular enjoyed was Bryan Sykes' Adam's Curse. See chapter 11, The Separation of the Sexes. Fred Hsu 16:00, 25 November 2006 (UTC)

Malicious Edit[edit]

Note the following sentence from the article as it stands: "A mitochondrion contains inner and outer Mac is pimp and he drinks orange juice. membranes composed of phospholipid bilayers and proteins."

I'm not a wiki-maven. Please re-edit and punish the offending interloper according to local custom. 16:16, 9 December 2006 (UTC)Freemount

That graffiti was erased back on 7 December 2006 at 14:24 (UTC). -R. S. Shaw 20:16, 9 December 2006 (UTC)

American or British spelling?[edit]

This article seems to be split fairly evenly between British and American spellings. My observation is:

oxidising 1
colour 1
analyse 1
oxidises 1
synthesize 1
organization 1
specialized 1
centers 1

We should settle on one of them, I would think. -R. S. Shaw

Just follow the guidelines at Wikipedia:Manual_of_Style#National_varieties_of_English. The general guideline is that its inevitable and to not worry about it. --Eean 05:06, 23 December 2006 (UTC)
Ok, following the guidelines, the spelling should be consistent and use the dialect of the first contributor. The first version used American spelling (e.g. "catalyze"), so I'll update the article to be consistent with this. -R. S. Shaw 00:20, 24 December 2006 (UTC)

Topics from 2007[edit]

"new mitochondria are synthesized"???[edit]

How are new mitochondria "synthesized"? 04:55, 13 May 2007 (UTC)

Through binary fission, just like prokaryotes in general. --arkuat (talk) 02:20, 4 July 2007 (UTC)

Converting NADH and NADPH into ATP?[edit]

Mitochondria are sometimes described as "cellular power plants," because they churn out energy for the cell by converting NADH and NADPH into ATP via the process of oxidative phosphorylation.

Firstly, I'm under the impression that in oxidative phosphorylation NADH and NADPH are not converted into ATP, ADP is. Secondly, NADPH doesn't take part in oxidative phosphorylation. Am I splitting hairs or just plain wrong? - Quirk 11:36, 15 May 2007 (UTC)

The page has been vandalised (or updated but some one who does not fully understand the process) but no one noticed. This is the classic problem with wikipedia. I'll try and tease out the bad edits from the more recent good edits. David D. (Talk) 12:58, 15 May 2007 (UTC)
Here is the problem edit.[2] appears to be a good faith attempt to make it livelier. I could do without the churn out imagery. David D. (Talk) 13:00, 15 May 2007 (UTC)

Power plant analogy[edit]

Mitochondria are sometimes described as "cellular power plants," because they churn out energy for the cell by converting NADH and NADPH into ATP via the process of oxidative phosphorylation.

Textbooks have been repeating that statement for a long time, "Mitochondria are the powerplant of the cell", or "Mitochondria are the powerhouse of the cell." Seems to me that mitochondria are less like a powerplant than they are like a refinery. A car engine is a powerplant; it takes in fuel and puts out power. A nuke plant is a powerplant; it get up steam and then produces electric power. A refinery takes in one kind of fuel and puts out a higher octane kind, pretty much like a mitochondrion does.Richard8081 21:50, 4 July 2007 (UTC)

This is an interesting discussion but leads us down the path of original research. Or do you have a citation where this is discussed? Personally, I would argue that the refinary argument is flawed in the sense that the fuel (hydrocarbons) is not actually changed, just purified. The powerplant analogy seems more apt. A typical powerplant will take potential energy, in the form of water (hydro), gas or coal, use it in the powerplant and convert it to a new form of useful energy; electricity. For mitochondria, substitute reduced molecules for coal and electricity for ATP. The proton gradient is fairly analogous to the steam or water that is used to drive the turbines (which are analogous to ATP synthase). Overall this is quite a robust analogy. David D. (Talk) 15:25, 5 July 2007 (UTC)

Just to make sure I got what you said there: the proton gradient of a mitochondrion is analogous to steam or water used to drive a turbine, you say. So the proton gradient is not stored electrical energy, like a capacitor? No? Richard8081 18:33, 16 July 2007 (UTC)

It depends what kind of analogy is being used. If you use electricity to pump water up to a higher lake (at night during low demand) and then reuse it to drive the turbine during the day to generate more electricity then this works. Now whether ATP is analogous to electricty as asked below is defintiely debatable. Hydrogen may be better. But a turbine producing hydrogen directly does not work as well in the analogy. David D. (Talk) 21:29, 16 July 2007 (UTC)

You ended saying that saying that ATP is "analogous to electricity". ATP is the epitomy of stored chemical energy. A mitochondrion uses electron transport down a voltage gradient to synthesize ATP, yes indeed, so it definitely is an electrical or electronic device, making electricity and making use of electricity to make ATP. 20:20, 16 July 2007 (UTC)

Electricity can be used to make hydrogen by electrolysis, so I can agree that ATP is more like hydrogen. But how does that fit into the analogy? What is the proton gradient? David D. (Talk) 21:25, 16 July 2007 (UTC)

The analogy is to a refinery: A refinery takes in crude oil and rearranges the molecules to yield compounds with a lot of available chemical energy, e.g. Diesel fuel, gasoline and jet fuel. A mitochondrion takes in glucose (or similar highly reduced biomolecules) and produces compounds with a lot of available chemical energy, e.g. ATP. 00:34, 17 July 2007 (UTC)

But refineries don't rearrange molecules. They separate them by distillation. (see above where i mentioned to Richard that "I would argue that the refinary argument is flawed in the sense that the fuel (hydrocarbons) is not actually changed, just purified. ") David D. (Talk) 01:19, 17 July 2007 (UTC)

Catalytic cracking. 10:55, 17 July 2007 (UTC) hydrocracking, alkylation and catalytic reforming too Richard8081 11:21, 17 July 2007 (UTC)

Fair enough, I thought you were referring to distillation (I don't know too much about refineries). Even then, the carbon atoms in the start molecules are the same as in the product. Clearly the atoms in glucose are not the same ones that are present in ATP (from the short term perspective of mitochondrial function). I wonder if such an analogy may actually mislead students rather than clarify the role of the mitochondrion? Or am I missing something else here? 14:26, 17 July 2007 (UTC)

Is there an example of a "power plant" whose product is some chemical used as a source of readily available energy? No. The product of a power plant is some kind of power like electrical power; or steam; or mechanical power. We don't really need to analogize mitochondria at all. We're trying to familiarize the students with biological chemistry. We stick to the chemistry, and that's how we familiarize them with electronegativity of chemical bonds. The segue to electron transport in mitochondria comes in naturally, so now we have a good solid background to get them comfortable with electricity in living cells. Thus educated, our students would never mistake a normally functioning mitochondrion exporting compounds with a high energy (8 kcal ! for ATP) phosphodiester bond, for a power plant exporting, say, electric current. Now, we have to stop there for the students, at least most of them, because when you get into the electrical or electronic nature of mitochondria, well, that's a lot more to try and explain, and pretty much impossible to analogize. When mitochondria build up a charge on one side of a membrane, by passing electrons along their electron transport chain and somehow creating a gradient of protons from one side to the other of the mitochondrial membranes, ie across the membrane, well there you have the electrical, or electronic nature of life. And if you look at a picture of those mitochondria in vivo, in situ, they are all hooked together physically -- they're networked. But we'll suffice it to say that SOMEHOW in the mitochondrial membranes the energy in reduced food molecules -- reduced meaning having lots of hydrogen stuck to the carbon atoms -- is "conserved" as high energy phosphodiester bonds e.g. in ATP; and we'll skip for now the role of electricity in how we think that is being accomplished. Certainly the students don't need to know it; what they really need to comprehend is this grand concept of energy conservation in living cells -- where does the food really go? Enough about the analogy, though. Most likely most other folks don't know much about refineries either; or power plants. They can look both of them up in Wikipedia, though! 04:54, 18 July 2007 (UTC)

My only point was that the refinery analogy is worse than the power plant analogy. No analogy is perfect and I'd be happy with no analogies. David D. (Talk) 14:16, 18 July 2007 (UTC)

Dudes the first paragraph[edit]

Ok I think it was a stupid mistake. It says they are the power houses of cells twice. (talkcontribs) 22:18, 18 May, 2007.

role in cancer and aging, ability to convert light into metabolic energy[edit]

This provides info on very interesting new research. --Espoo 18:15, 27 June 2007 (UTC)

Disease related functions[edit]

I've removed the section on this, as I can't find anything relevant to it in PubMed:

Another study by Professor Peter Piper, a professor of molecular biology and biotechnology, has found that the additive E211 or sodium benzoate, found in soft drinks and sauces, damages the mitrochondria. As stated: "The mitochondria consumes the oxygen to give you energy and if you damage it - as happens in a number of diseased states - then the cell starts to malfunction very seriously. And there is a whole array of diseases that are now being tied to damage to this DNA - Parkinson's and quite a lot of neuro-degenerative diseases, but above all the whole process of ageing."[1]

If anybody can find the publication this report is based on, that would be great. I think the author is "Piper PW" Tim Vickers 03:27, 6 September 2007 (UTC)

Dear Tim Vickers I have reverted your edit and placed some references following the reference of the article. Please do not just delete controversial statements but place fact tags, otherwise edits get forgotten and not properly referenced (my own experience). Please verify the authenticity of the references.

Teardrop onthefire 08:45, 6 September 2007 (UTC)

I'm still worried about the accuracy of this section. I looked at that EJB paper (from 2003) and it has nothing to do with mitochondria. It deals with how yeast can become resistant to benzoate and the influence of aromatic amino acid metabolism on this phenotype. Furthermore, the news reports are from 2007, so are unlikely to be talking about a publication from four years ago. The first reference in the list above (the 2001 review) says ATP depletion is caused by inhibition of glycolysis, with the inhibition of oxidative phosphorylation playing a secondary role. This is why I removed the section, it just does not appear to fit the published literature.
As a secondary comment, why should we be concerned that a food preservative kills food spoilage organisms at the concentrations used to prevent spoilage in food? I don't see the relevance of that rather predictable result to human toxicology. Tim Vickers 15:36, 6 September 2007 (UTC)
I agree with Tim here, this whole section is far too detailed and speculative to be useful. We should be talking about mitochiondrial myopathies in this section, not poisons. Connecting mito function, or lack of it, with diseases. David D. (Talk) 20:16, 6 September 2007 (UTC)
I've rewritten this section to accurately reflect the source, but this is really just wild-eyed speculation from the newspaper. I can't see how this scare story belongs in the main article on mitochondria. Tim Vickers 20:29, 6 September 2007 (UTC)

I understand your concerns, I have looked for some other sources:

Apperently there was a survey on this, the danger would be minimal, but still there is no absolute certainty. Please check the source. Teardrop onthefire 13:12, 7 September 2007 (UTC)

Well this link is completely different to Pipers claims. This says that drinks with benzoate salts can become contaminated with benzene. What does that have to do with mitochondrial disease? Considering this article barely touches on drugs such as rotenone, cyanide or other respiratory chain inhibitors why would we include this, and especially why in the disease section? What about the genetically inherited myopathies, we have nothing about those diseases. What about the slimming drugs like DNP that short circuit the mitochondria? That seems more relevant but again none of these relate to diseases as such. As far as I can tell the only reason Piper is talking about diseases is because that is how he gets funding. The reality is that his links are tenuous at best. Certainly not worthy of an entry in a very general introduction to mitochondria. David D. (Talk) 13:23, 7 September 2007 (UTC)
I have no intention of keeping the text in at all costs, I am just providing sources, I will let the interpretation to the experts, I am no microbiologist. I will be on the lookout if the study is published after all. Teardrop onthefire 14:01, 7 September 2007 (UTC)

I believe the next source is related to the research. Please excuse me if it is not.

Teardrop onthefire 14:44, 7 September 2007 (UTC)

Excellent, that's good work. That is the study we've been looking for. However, I had a look at it and it actually contains no data on health risks in humans. This is mentioned as a possibility that should be examined in the future in the article's discussion.
"These experiments on yeast cells set the stage for further study of whether weak organic acid food preservatives exert pro-oxidant effects on such epithelia. With the implication of oxidative stress in certain genetic diseases of humans [13, 14 and 42] and in the development of a wide range of different cancers [43, 44 and 45], the potential for weak organic acid food preservatives to act as pro-oxidants in humans should probably be reexamined, if only to reassure the public of the complete safety of these compounds."
This confirms my idea that this is a speculative proposal based on extrapolating from yeast to people. If nobody objects, I'm going to remove the speculation from the article and replace it with some cases where disease is known to be associated with mitochondrial dysfunction in humans. Tim Vickers 14:53, 7 September 2007 (UTC)
That would be a distinct improvement. Please do so. -R. S. Shaw 00:20, 8 September 2007 (UTC)
Done. Tim Vickers 02:50, 8 September 2007 (UTC)

Topics from 2008[edit]


hi everyone! i am doing a science project and i was wondering what the function is for a mitochondrea?

Hi there, see Mitochondrion#Function in this article. Tim Vickers (talk) 21:28, 4 November 2008 (UTC)

Retrofit topic year headers/subpages[edit]

12-Nov-2008: I have added subheaders above as "Topics from 2005" (etc.) to emphasize the dates of topics in the talk-page. Older topics might still apply, but using the year headers helps to focus on more current issues as well. The topic-year boundaries were located by searching from bottom for the prior year#. Afterward, I dated/named unsigned comments and moved 4 entries (including "Endosymbiotic theory" & "Mitochondrial pH") into date order for 2002, 2006 & 2007.
Then I added "Talk-page subpages" above the TOC. -Wikid77 (talk) 06:10, 12 November 2008 (UTC)

Topics from 2005[edit]


This article has been accepting a number of "1 line updates" over its history, and has become somewhat cluttered. Additionally, many of the entries are redundant ("cristae" were described a number of times, for example), and a number of the entries were opaque to a lay reader (such as unexamplined references to "alpha-proteo bacteria" and "matrix-targeting sequences", for example). I decided to undertake a large rewrite of this article, with the goals of reorganizing the information, and making it fully accessible to, say, a motivated middle school reader. Entries of more complexity should be pushed into specialized articles on the subject. – ClockworkSoul 17:44, 18 Mar 2005 (UTC)

Organisinisation of the mitochondrion associated articles[edit]

I've been looking at the articles that stem from this one and I think that we should consider the following changes:

--nixie 23:09, 10 Apr 2005 (UTC)

Topics from 2006[edit]

Mito and ATP Synthase[edit]


Mito actually are kind of threadlike, they're also round. I've seen lots of electron micrograph images in my cell class, my impression is that they are pretty fluid. But, i think it mostly depends on the cell. Mito in the axon of a neuron are going to arranged differently than those in a liver cell, etc.

Also, the image in the article depicts ATP synthase as floating around in the matrix. It's actually a transmembrane protien, actually that is essential to its function, as it is motivated by the flow of the H+ that have been pumped across the membrane.

Peace, --FoodRiot 04:53, 22 May 2006 (UTC)FoodRiot

This is a Good Article[edit]

After review, I've determined this article to meet the qualifications for good article status. Remember to keep up with the references for future edits, and continue to use the inline style whenever possible.

I do have a comment about the images. The two images seem to be roughly the same. One is just a very simple version of the other, but doesn't seem to add much in the way of its own information. I noticed a discussion a few months ago about some new images. What happened to those? The combination of a 'very simple' graphic and a 'more realistic' graphic makes sense.

Keep up the good work, folks. Remember, when making small changes, to read the surrounding paragraphs, and make small edits as necessary to make sure that your addition 'flows' into the rest of the article. It is easy for articles to end up as long lists of distinct sentences, if you take the time to read the entire paragraph, and 'flow' your addition in, it makes things much more readable. Feel free to message me on my talk page if you have any questions about my promotion rationale. Phidauex 17:31, 11 July 2006 (UTC)

Yeah! pschemp | talk 17:40, 11 July 2006 (UTC)
Very nice work! congrats to the editors that made this happen, you know who you are. ++Lar: t/c 19:33, 11 July 2006 (UTC)

This article may be a good article by editorial standards; the problem is that it doesn't have much to do with living breathing mitochondria. For starters, let's get a picture in the article of the network of mitochondria that you see when you do selective staining, taking a look at the mitochondria as they reside in cells -- in vivo, more or less in situ; well, they're alive, anyway. I am pretty sure that such pictures have been around for about twenty years now, since around 1987 or so.Richard8081 00:00, 4 July 2007 (UTC)

Aren't mitochondria more like a refinery than like a powerplant? Richard8081 00:00, 4 July 2007 (UTC)


I came to this article to look up the influence of Mitochondrial DNA on aging an I notice that it isn't in the article. Is this deliberate because the research is too new, or is it just because non one has added it in yet? Theresa Knott | Taste the Korn 22:56, 13 July 2006 (UTC)

  • MtDNA like all DNA accumulates mutations - this has been linked to aging (i.e the older you are the more mutations there will be - which is espeically apparent in long-lived tissues like the brain; mitochondria also don't work as efficiently with age (in part due to accumulated mutations) which can also cause phenotypes) - but from a quick look at PubMed no one has really shown how MtDNA degeneration directy affects aging.--Peta 23:10, 13 July 2006 (UTC)
    • I read something in the new scientist (I don't have the copy in question any more) that stated that recent research linked mitochondrial DNA directly to aging. After all short lived tissues like skin also age. I didn't understand the mechanism though :-( Theresa Knott | Taste the Korn 23:39, 13 July 2006 (UTC)

He we go - a little light reading for anyone who is interested.

Review paper [3] "Several hypotheses suggest that defective mitochondria contribute to, or are responsible for, ageing. Recent observations indicate that mitochondria in an old organism differ in many respects from those in a young organism."

Letters to Nature[4] "Our results thus provide a causative link between mtDNA mutations and ageing phenotypes in mammals."

I don't know enough biology to write anything up myself I'm afraid What you you guys think? Theresa Knott | Taste the Korn 23:49, 13 July 2006 (UTC)

Later work on the mutator mouse (from the second article you cite) proposes that the aging phenotype is caused by respiratory chain failure rather than the mutations; suggesting that loss of mitochondrial function is a major causal factor in aging rahter than mutations in mtDNA. To quote a letter to Science (310:411) - "Whether the rate of aging depends critically on mitochondrial mutations is still very much an open question".
We should probably add a mention of the theory, but at this point is is just a theory.--Peta 00:20, 14 July 2006 (UTC)

I agree with Peta's remarks. I followed a course on biology of ageing some years ago, and it's clear that ageing cannot be attributed to a single process, there are many important, different processes going on. Please consider this when writing about the research. Jens Nielsen 13:13, 14 July 2006 (UTC)

That's all I'm asking for. A brief mention of the theory with a statement that it's still a top[ic or research and debate. Theresa Knott | Taste the Korn 20:23, 15 July 2006 (UTC)

Peer Review[edit]

This article has been listed at Peer Review. Please take the time to read the suggestions made at Wikipedia:Peer review/Mitochondrion and improve the article if you can. The biggest issue is references, anyone who can contribute in that area would be appreciated. I think that this article can become a Featured Article with just a little more work, so let's do it. pschemp | talk 01:46, 17 July 2006 (UTC)

mitochondria in forensics[edit]

I propose the creation of a new section for the use of mitochondrial DNA in forensics. Mitochondrial DNA can be used to determine indentity when nuclear DNA is not available. If there are no objections, I will get started on this soon! Lauren 15:47, 29 August 2006 (UTC)

25% of the cell's cytoplasm[edit]

'Usually a cell has hundreds or thousands of mitochondria, which can occupy up to 25% of the cell's cytoplasm.' Can anyone cite that? Also- by weight, volume, or some other, more esoteric, measure?

That's probably easy: Molecular Biology of the Cell, by Alberts et al. Here's the book's web site: I glanced through my copy, but couldn't find those numbers--but the book is over 1000 pages long, so it's not surprising I didn't find it. This is one of those numbers I see quoted in the literature all the time, but without citation. :( As for the 25%, that is probably by both weight and volume--I don't expect there to be huge differences between cytosolic density and mitochondrial density, and that number is probably fairly rough anyway. ~Doc~ EquationDoc 05:08, 10 November 2006 (UTC)

Topics from 2007[edit]

Mitochondrial pH[edit]

Articles always mention the fact that protons are driven accross the membrane to drive ATP formation, but what is the actual pH accross these membranes? I'm very interested to hear about how much this varies, because, of course, pH is integral to protein structure. When we add something that uncouples phosphorylation, like dinitrophenol, would this affect the mitochondrial proteins? There's a massive proton gradient, surely there's a pH gradient too? Does this change intracellular pH in the local vicinity of the mitochondrion too?Jph53 17:05, 14 March 2007 (UTC)

Good point. FYI the pH gradient is 1 (10 fold concentration difference). In chloroplasts it is a whopping 4 pH units difference between the lumen (pH4) and the stroma (pH8). Both electrochemical gradients drive the ATP synthase and actually have about the same energy potential despite the large concentration difference in protons. The mitochondrial inner membrane has a negative charge on matrix side compared to the inner membrane space side. This charge makes up the difference in the mitochondria such that the mito and chloroplast proton gradients have roughly the same electrochemical potential when ATP synthesis is active. There is no charge across the choroplast thylkoid membrane. David D. (Talk) 18:26, 14 March 2007 (UTC)

Mitochondrial number and volume[edit]

The concept that there is a typical eukaryotic cell with 2000 mitochondrion is confusing. Mitochondrial number is specific to tissue and organism type. I suggest that this line be replaced with something like "Mitochondrion number varies immensely according to organism and tissue type. Many cells possess only a single mitochondrion, while others can contain several million. Molecular Biology of the Cell, Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter, ISBN 0815332181 --Spamburgler 02:30, 24 April 2007 (UTC)

Is this "single mitochondrion" a filamentous network of, well, mitochondria? Richard8081 20:31, 15 August 2007 (UTC)

Well? Anyone? Richard8081 (talk) 13:45, 10 June 2008 (UTC)

The kinetoplast in protozoa like Trypanosoma brucei is a single mitochondrion with a single continuous mitochondrial matrix. It extends the length of the cell. Tim Vickers (talk) 16:10, 10 June 2008 (UTC)

fungus or protozoa[edit]

Cryptosporidium is not a fungus —The preceding unsigned comment was added by (talk) 22:08, 6 May 2007 (UTC).

"Death Center"[edit]

I was just reading a New Scientist article (;jsessionid=LCNFCHIBIPGB ) and it had an interview where he states that they are hypothesising that the mitchondria are also the "death center" for the cell and can trigger death in a variety of circumstances. Is this worth a mention? just thought i would bring it to attention... Helmet Shell 13:28, 15 October 2007 (UTC)

Resubmission for featured article status?[edit]

Anybody know what it will take to resubmit this for FA review? There have been huge improvements since July 2006 when it was reviewed, and nearly all the criticisms in the review have been implemented. The number of references has gone up 10-fold since then as well. Sedmic 16:37, 4 November 2007 (UTC)

First check the Featured Article criteria, and if the article has met them, you can submit it for review at WP:FAC. –panda 16:12, 1 December 2007 (UTC)

I think this article may meet criteria for FAC. I just submitted it for peer-rereview. After working on this for a while, I'm looking for suggestions on new areas to improve within the article to get it to FA status. What else should be in this article to make it complete without being unnecessarily long? Thanks! Sedmic 21:22, 7 December 2007 (UTC)

Article nominated for WP:FAC. I don't see much more coming in the way of peer review. Sedmic 17:45, 16 December 2007 (UTC)

A few inaccuracies/unclarities[edit]

Even though the article for the large part is very good, it includes a few points that could be clarified better.

  • As the mitochondrial content of a cell is in a constant flux of fusing and division (example review[5], visual representation here [6]), it might be better to refer to it as "the mitochondrial network". Likewise, it is usually more accurate to use the copy-number of the mitochondrial DNA in the cell as a whole as a measure of mitochondrial content. "MtDNA/mitochondrion" is a meaningless measure due the mentioned dynamics of the mitochondrial network.
  • When talking about the mitochondrial genome, it should be made clear that it is the human one being talked about. This as other species have fewer or more genes in mtDNA, and the mtDNA of different species is dramatically different in lenght (plant mitochondrial DNA especially are often very large), ie mtDNA is not by definition ~16kb. There is also a wierd choice of words in this section "and many chromosomes are circular". Almost all mtDNA is circular, linear mtDNA must be said to be the rare exeption [7].
  • It has recently been shown by several groups that increased reactive oxygen species is not coupled with mitochondrial mutations linked with ageing. (example[8]).

Any comments? --Lensor (talk) 09:57, 26 November 2007 (UTC)

These are all really good comments. I'd invite you to just make the changes yourself and any other corrections/copy editing. Is there any reason why you'd prefer not too? David D. (Talk) 10:01, 26 November 2007 (UTC)
None really, just that they might be viewed as controversial (especially the ageing comment), and I wanted to get comments first.--Lensor (talk) 10:04, 26 November 2007 (UTC)
I think the PNAS paper you linked is great. I missed it when I originally wrote the paragraph on ROS. There's a lot of controversy still, but this paper certainly deserves mention. I'm adding it in now. Please alter/add if you think it needs further clarification or you disagree with what it says. Sedmic 15:38, 7 December 2007 (UTC)


>> "These porins form large aqueous channels that permit the passage of molecules 5000 daltons or less."

  • The link to daltons goes to an article about a newspaper (I think. Not sure :). I'll fix the hatnote in a bit.
  • to make it easier to read to a dimwit like me, could perhaps the trailing clause read "... molecules that are 5000 daltons or less in weight"?

Thanks. -- Fullstop (talk) 20:44, 16 December 2007 (UTC)

Thanks for the suggestions. I moved the daltons link to Atomic mass units and changed the sentence as requested. Sedmic 00:43, 17 December 2007 (UTC)

external links[edit]

i removed the three above since they should probably be cited in the text at the apropriate place, if appropriate, rather than exist as external links. David D. (Talk) 21:23, 16 December 2007 (UTC)

I added the PLOS Bio article which that summary referred to in to the main page. The pages are interesting summaries with possibly useful bibliographies, but I don't know that they necessarily add anything new other than more papers to read if interested? Sedmic 00:39, 17 December 2007 (UTC)
I added the mitochondria and aging link as a reference in the aging section at the end.--Xris0 (talk) 03:47, 11 May 2008 (UTC)


There is a genome section in this article and two separate articles on mitochondrial DNA (mtDNA) and mitochondrial genome which was proposed for a merge with mtDNA. Which one should be the main article for the genome section in this one? - tameeria (talk) 19:34, 30 December 2007 (UTC)

I agree that mitochondrial DNA and mitochondrial genome should probably be merged. As it stands, I favor mitochondrial DNA as the main linked article from mitochondria because it has more facts and is better sourced. However, there are many details in the mitochondria section on genome that are missing from the mitochondria DNA article. Maybe some of these items can be transferred in the future ... Sedmic 17:31, 1 January 2008 (UTC)

CMS in plants[edit]

Mitochondria can be involved in cytoplasmic male sterility in plants. This should probably at least be mentioned in the article. - tameeria (talk) 19:45, 30 December 2007 (UTC)

Topics from 2008[edit]

Apparent Contradiction in Origins section[edit]

At the moment, it says:

A few groups of unicellular eukaryotes lack mitochondria: the microsporidians, metamonads, and archamoebae.[35] These groups appear as the most primitive eukaryotes on phylogenetic trees constructed using rRNA information, suggesting that they appeared before the origin of mitochondria. However, this is now known to be an artifact of long branch attraction – they are apparently derived groups and retain genes or organelles derived from mitochondria (e.g., mitosomes and hydrogenosomes).[1] There are no primitive eukaryotes today that lack mitochondria.

The first bolded sections appears to contradict the second, can someone who knows which is correct edit out the incorrect section? Or resolve the apparent contradiction - JackAidley (talk) 15:22, 8 January 2008 (UTC)

Mitochondrion image[edit]

It would be useful to know what tissue the mitochondrion image in the lede came from, and what size the organelle is (no scale is provided or statement of magnification). Also, the resolution of that image is disappointing, too low to show details of the cristae, or relationships between inner and outer membranes. Any chance of a better picture, or a better version of the same one with more details of origin and a scale? Plantsurfer (talk) 10:04, 6 September 2008 (UTC)

See Category:Mitochondria. Tim Vickers (talk) 15:58, 6 September 2008 (UTC)
OK Thanks, that'll do nicely Plantsurfer (talk) 16:38, 6 September 2008 (UTC)

Copy number[edit]

The article now mentions that the number of mitochondria per cell varies from thousands (in muscle cells) to one. Someone who has relevant sources please expand on this, and include plants. This is a point of interest to readers of several medical articles, including Gout. Other information of interest, apart from copy number, are the variations in total DNA and RNA content of mitochondria. --Una Smith (talk) 14:02, 24 October 2008 (UTC)

I was thinking that the entire "organization and distribution" section could do with a rewording, This as what we today know about the organization of mitochondria not as discrete units, but as a constantly fusing and dividing network, makes it in essentially pointless to talk about mitochondrial copy number. A better measuring unit is mitochondrial DNA copy number. Alternatively mitochondrial mass.--Lensor (talk) 13:28, 1 April 2009 (UTC)

Retrofit topic year headers/subpages[edit]

12-Nov-2008: I have added subheaders above as "Topics from 2005" (etc.) to emphasize the dates of topics in the talk-page. Older topics might still apply, but using the year headers helps to focus on more current issues as well. The topic-year boundaries were located by searching from bottom for the prior year#. Afterward, I dated/named unsigned comments and moved 4 entries (including "Endosymbiotic theory" & "Mitochondrial pH") into date order for 2002, 2006 & 2007.
Then I added "Talk-page subpages" above the TOC. -Wikid77 (talk) 06:10, 12 November 2008 (UTC)

Technical article denied FA status[edit]

12-Nov-2008: I noticed the article was denied "Featured-article" status due to several sentences containing more than 3 technical terms. Based on that rejection, few tech articles can qualify. Would "Quadratic equation" be denied FA-status unless equation and algebra were also explained in that article to avoid using outside technical terms? Meanwhile, "Mitochondrion" is a very good tech article, but I can't see it ever becoming "Introduction to Mitochondrion" for the beginner. Seems like the FA-criteria tend to exclude tech articles that have lots of details. -Wikid77 (talk) 06:10, 12 November 2008 (UTC)

Created talk-page archive[edit]

12-Nov-2008: I just now created Talk:Mitochondrion/Archive prior talk (after 6 years of entries), and moved 25 older topics (60%) to that file, such as 2003 content debates & "need help with science project" or such. The entries there are in the same order, grouped under "Topics from 2005" (etc.), but it might be years before more need to be moved there. -Wikid77 (talk) 06:59, 12 Nov 2008

Why create an archive? Was there something dated about the discussions? Put it this way: The Archivist here = Wikid77 knows a lot about Wikipedia practices; where is the rulebook or recommendations about putting stuff in an archive? Richard8081 (talk) 15:52, 21 April 2009 (UTC)

It's pretty standard when the page starts to get long. There is a link at the top of the page. Most people know to look for the talk page archive link at the top. David D. (Talk) 14:40, 23 April 2009 (UTC)

English, please.[edit]

I apologise to have to ask you to do this, but I scarecly understood a word of the text. I am a student and I am looking up the cells for my science class. I don't have the best range of vocabulary, but it's rather large compared to some of the people at my school. I know if I barely understood the secton on Mitochondria, nor will my fellow students. Many people turn to Wikipedia when they are in need of vocabulary help. But how is it suppost to help them when they can scarecly understand what it is speaking of? In the highest regards for the owner of this website, i write this. —Preceding unsigned comment added by (talk) 13:45, 23 April 2009 (UTC)

An example would be useful. David D. (Talk) 14:38, 23 April 2009 (UTC)

Topics from 2009[edit]

PMID 19716394 -- "exercise, particularly aerobic exercise, activates mitochondriogenesis in the young animal but its effects on mitochondrial biogenesis in the old animal are doubtful."[edit]

Mitochondrial biogenesis in exercise and in ageing.

Viña J, Gomez-Cabrera MC, Borras C, Froio T, Sanchis-Gomar F, Martinez-Bello VE, Pallardo FV. Department of Physiology. University of Valencia, School of Medicine, Spain.

Adv Drug Deliv Rev. 2009 Aug 28. [Epub ahead of print]

Mitochondrial biogenesis is critical for the normal function of cells. It is well known that mitochondria are produced and eventually after normal functioning they are degraded. Thus, the actual level of mitochondria in cells is dependent both on the synthesis and the degradation. Ever since the proposal of the mitochondrial theory of ageing by Jaime Miquel in the 70's, it was appreciated that mitochondria, which are both a target and a source of radicals in cells, are most important organelles to understand ageing. Thus, a common feature between cell physiology of ageing and exercise is that in both situations mitochondria are critical for normal cell functioning. Mitochondrial synthesis is stimulated by the PGC-1alpha-NRF1-TFAM pathway. PGC-1alpha is the first stimulator of mitochondrial biogenesis. NRF1 is an intermediate transcription factor which stimulates the synthesis of TFAM which is a final effector activating the duplication of mitochondrial DNA molecules. This pathway is impaired in ageing. On the contrary, exercise, particularly aerobic exercise, activates mitochondriogenesis in the young animal but its effects on mitochondrial biogenesis in the old animal are doubtful. In this chapter we consider the interrelationship between mitochondrial biogenesis stimulated by exercise and the possible impairment of this pathway in ageing leading to mitochondrial deficiency and eventually muscle sarcopenia.

PMID 19716394 —Preceding unsigned comment added by (talk) 15:08, 11 October 2009 (UTC)

Mitochondria changes in human muscle after prolonged exercise, endurance training and selenium supplementation[edit]

Zamora AJ, Tessier F, Marconnet P, Margaritis I, Marini JF.

Mitochondria changes in human muscle after prolonged exercise, endurance training and selenium supplementation.

CNRS, Faculté des Sciences du Sport, Université de la Méditerranée, Marseille, France.

Eur J Appl Physiol Occup Physiol. 1995;71(6):505-11.Links

The functional and structural responses to acute exercise (E) and training, (T) with or without selenium supplementation (Sel), were investigated in a double-blind study on 24 young male subjects. The Sel or the placebo were given over 10 weeks of an endurance training programme. Prior to the programme and on its conclusion muscle biopsies were taken from the vastus lateralis muscle before and after an exhausting treadmill test of maximal endurance capacity (Capmax). The muscle samples were examined by electron microscopy to make a quantitative analysis of the mitochondria population in the muscle fibres. The number of mitochondria per area (QA) and the relative surface occupied by the total mitochondria profile area (AA) were estimated. The mean area per mitochondrion (â) was obtained by the quotient AA/QA. The effects of the isolated or combined independent variables T, E and Sel were analysed by nonparametric tests. Training induced significant increases in both QA (30%, P < 0.001) and AA (52%, P < 0.001), without changing â; T + Sel produced a slight rise of AA (27%, P < 0.001), which resulted in larger (24%, P < 0.001) â. The E produced an enlargement of â resembling swelling. This phenomenon was also found for the combinations E + T and E + T + Sel, but it was then far more pronounced in E + T. The training effects observed are in agreement with previous descriptions. In contrast, the changes observed after acute exercise seem to indicate a remarkable short-term plasticity of muscle mitochondria. The results in Sel would seem to suggest a dampening effect of the selenium on the mitochondria changes, both in chronic and acute exercise. The mechanism of this action on mitochondrial turnover is uncertain, but might be related to a higher efficiency of the selenium-dependent enzyme glutathione peroxidase.

Regulation of mitochondrial biogenesis critical to healthy aging[edit]

Mitochondrial biogenesis and healthy aging.

López-Lluch G, Irusta PM, Navas P, de Cabo R.

PMID 18662766

Exp Gerontol. 2008 Sep;43(9):813-9. Epub 2008 Jul 9.

Centro Andaluz de Biología del Desarrollo, Universidad Pablo de Olavide-CSIC, Carretera de Utrera Km 1, 41013 Sevilla, Spain.

Aging is associated with an overall loss of function at the level of the whole organism that has origins in cellular deterioration. Most cellular components, including mitochondria, require continuous recycling and regeneration throughout the lifespan. Mitochondria are particularly susceptive to damage over time as they are the major bioenergetic machinery and source of oxidative stress in cells. Effective control of mitochondrial biogenesis and turnover, therefore, becomes critical for the maintenance of energy production, the prevention of endogenous oxidative stress and the promotion of healthy aging. Multiple endogenous and exogenous factors regulate mitochondrial biogenesis through the peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha). Activators of PGC-1alpha include nitric oxide, CREB and AMPK. Calorie restriction (CR) and resveratrol, a proposed CR mimetic, also increase mitochondrial biogenesis through activation of PGC-1alpha. Moderate exercise also mimics CR by inducing mitochondrial biogenesis. Negative regulators of PGC-1alpha such as RIP140 and 160MBP suppress mitochondrial biogenesis. Another mechanism involved in mitochondrial maintenance is mitochondrial fission/fusion and this process also involves an increasing number of regulatory proteins. Dysfunction of either biogenesis or fission/fusion of mitochondria is associated with diseases of the neuromuscular system and aging, and a greater understanding of the regulation of these processes should help us to ultimately control the aging process. —Preceding unsigned comment added by (talk) 19:06, 13 October 2009 (UTC)

Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency[edit]

López-Lluch G, Hunt N, Jones B, Zhu M, Jamieson H, Hilmer S, Cascajo MV, Allard J, Ingram DK, Navas P, de Cabo R.

Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency.

PMID: 16446459

Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1768-73. Epub 2006 Jan 30.

Centro Andaluz de Biología del Desarrollo, Universidad Pablo de Olavide, 41013 Sevilla, Spain.

Age-related accumulation of cellular damage and death has been linked to oxidative stress. Calorie restriction (CR) is the most robust, nongenetic intervention that increases lifespan and reduces the rate of aging in a variety of species. Mechanisms responsible for the antiaging effects of CR remain uncertain, but reduction of oxidative stress within mitochondria remains a major focus of research. CR is hypothesized to decrease mitochondrial electron flow and proton leaks to attenuate damage caused by reactive oxygen species. We have focused our research on a related, but different, antiaging mechanism of CR. Specifically, using both in vivo and in vitro analyses, we report that CR reduces oxidative stress at the same time that it stimulates the proliferation of mitochondria through a peroxisome proliferation-activated receptor coactivator 1 alpha signaling pathway. Moreover, mitochondria under CR conditions show less oxygen consumption, reduce membrane potential, and generate less reactive oxygen species than controls, but remarkably they are able to maintain their critical ATP production. In effect, CR can induce a peroxisome proliferation-activated receptor coactivator 1 alpha-dependent increase in mitochondria capable of efficient and balanced bioenergetics to reduce oxidative stress and attenuate age-dependent endogenous oxidative damage. —Preceding unsigned comment added by (talk) 19:17, 13 October 2009 (UTC)

Replication and inheritance and mitochondrial biogenesis[edit]

Hi, I am not a domain expert here, but one thing that this article and this section in particular doesn't seem to cover in any appreciable depth is the mitochondrial life cycle w.r.t. the host cell. It does discuss the mammalian (well actually human but I generalised this to mammalian) mitochondrial life cycle but doesn't really go into the mitochondrial biogenesis. Just a quick search (PubMed: mitochondria biogenesis) shows that this research field is quite active. For the lay person who is interested in this some typical figures would be very useful set this in context: typical numbers of mitochondria per cell, and their half-lives (by cell type). Also a reordering to collect related sentence would also help so the first para could become:

Mitochondria divide by binary fission similar to bacterial cell division; unlike bacteria, however, mitochondria can also fuse with other mitochondria.[REF]. The regulation of this division differs between eukaryotes. In many single-celled eukaryotes, their growth and division is linked to the cell cycle. For example, a single mitochondrion may divide synchronously with the nucleus. This division and segregation process must be tightly controlled so that each daughter cell receives at least one mitochondrion.
By contrast, the mitochondria in most animal cells are apparently randomly distributed to the daughter cells during the division of the cytoplasm, and the numbers of mitochondria vary according to the energy needs of the cell, with the mitochondria continually being replaced during the life of the cell. When the energy needs of a cell are high, mitochondria grow and divide. When the energy use is low, mitochondria are destroyed or become inactive. For example, there are approximately X mitocondria in a human liver cell with an average live of Y days and P in a heart muscle cell with an average life of Q days[REF].

As to the references, my problem not knowing my way around the published literature is that there are hundreds of related article, and a few popular science reviews (which tend not cite RS). So I have come across PMID 3170646, PMID 4674506, PMID: 885911, but I am sure that a domain expert could massage this wording and fill the numbers / references. -- TerryE (talk) 19:12, 2 March 2010 (UTC)

Hi, did you notice this section: Mitochondrion#Organization_and_distribution? It contains numbers, although the discovery of the mitochondrial network (also mentioned in this section) makes any mention of a number of separate mitochondrial units per cell pretty useless. The only number per cell that makes sense IMO is the number of mtDNA molecules.--Biologos (talk) 12:02, 3 March 2010 (UTC)
I had come across this concept (of the mitochondria not being contained is this isolated pill-like lipid membrane typical of many bacteria) in reading some the PLoS articles (sorry but as much as my interest in this goes, it doesn't stretch to paying $34 for some 6 page article), and certainly in research over this last 10 years or so. However given that the impression given throughout this entire article is of this traditional view. Yes, there is one passing reference to "Often they form a complex 3D branching network inside the cell with the cytoskeleton" linking to one primary MEDRS, but that exposure could be best described as very subtle and understated :-) What is the prevailing consensus on this, BTW? Are there any decent secondary reviews by now? What does this by "complex branching network", do this mean that they share a common inner membrane, outer membrane or just anchored together by surface proteins? In the second and third cases unitary identity is meaningful. For me, this article leaves me asking more Qs than it answers. that's all. I could go on but that not the purpose of this talk page. -- TerryE (talk) 18:23, 3 March 2010 (UTC)
Indeed, that's a fascinating question: What sort of network IS it, that these mitochondria make with each other? Given that mitochondria are nanoscale tunnelling electronic devices, the picture of them as NETWORKED nanoscale tunnelling electronic devices is just intriguing; they could be doing all sorts of higher order operations. It is, after all, called ELECTRON transport, not different from what happens on a chip. (talk) 05:00, 28 March 2010 (UTC) This contribution is from Richard8081 who is temporarily separated from his password
It would be cool if the Mitochondrion article had a selectively stained photo of a cell showing the network of mitochondria. Richard8081 (talk) 10:32, 28 March 2010 (UTC)
(Previous formatting tidied) @R8081: Yes, the mitochondria like every living system use nanoscale devices (a.k.a. proteins, enzymes, ...) to carry out their processes. The components employed in the Krebs cycle are well understood. Yes, there has also been some recently published research showing that quantum effects are implicated in processes such as photosynthesis, but the assertion that the Mitochondria in their entirety are "...nanoscale tunnelling electronic devices..." is just OR. We need to await a valid MEDRS basis for any inclusion in this article.

What does "... the mitochondria in their entirety ..." mean? Richard8081 (talk) 05:59, 13 April 2011 (UTC)

"nanoscale devices aka proteins, enzymes" seems to have left out the "electronic" part. It's not original research (OR) that mitochondria accomplish electron transport; it's a well known fact of biology, I do believe; and a good subject for discussion. Richard8081 (talk) 00:26, 14 April 2011 (UTC)

I am also going to revert the removal by IP Unfortunately having looked at some of the relevant papers, it really is that obscure. Yes, this areas needs to be filled out, but this text does reflect some of the complexity here. If IP124 wants to start removing content then he /she should explain the justification in this talk page. -- TerryE (talk) 09:59, 29 March 2010 (UTC)

Article Cleanup[edit]

I am a reasonably experienced editor, but domain non-expert, interested in the Mitochondrion and related articles. I've been somewhat unsatisfied with the overall article structure for some time and I feel that it needs improving from an editorial rather than content perspective. For example the article has a number of daughter articles (eg. Outer mitochondrial membrane for the section Outer membrane) are based on a clone of content. However there seem to be three main problems:

  1. The cloned copy has only pulled across the text and not the corresponding references, leaving the daughter page unreferenced.
  2. Content has been added to the main article, but not the daughter so that the latter is different to the former rather than a superset.
  3. There are sometimes minor inconsistencies between the two versions.

I propose to clean up some of these, but given my non-expert status, I wanted to alert project members and get feedback before doing so. I have create this thread for this discussion. I'll leave it a week or so for comment before starting. (I've copied this post on the relevant project pages, but assume that any feedback/discussion will be here. -- TerryE (talk) 14:46, 4 May 2010 (UTC)

I am not sure what you mean by cleanup. My proposal would be to delete the daughter articles, at least the ones dealing with substructures of the mitochondrion, merge any additional content from the daughter articles with the main article and install redirects. Or is the size of the main article a problem?--Biologos (talk) 16:05, 4 May 2010 (UTC)
I will need to review the history and perhaps ask the original editor(s) re the rationale for creating the daughter articles. This main article is bubbling along at just under 62K, and so it is pretty unwieldy. Splitting off some of the daughter articles which drill down into a more detail than is currently in the main article has helped prevent the article going over the 64K advisory limit. Merging these detailed articles would make the article longer. However some are little more than place-holder clones with detail being added to the the main article rather than the daughter where it belongs. Perhaps I should do an analysis of the tree and make a more concrete suggestion here for discussion. TerryE (talk) 16:58, 4 May 2010 (UTC)
Most of the daughter articles don't really seem to be long enough, right now, to be separate, but based on {{Mitochondrial enzymes}} they might have potential for expansion. I don't think we should expand the main article much (it seems to be at roughly the level of detail that a reader would want to see, without clicking on a link). Kingdon (talk) 19:27, 17 May 2010 (UTC)

Should there be a reference to the "Hydrogen Hypothesis" under origins?[edit]

There is no direct reference to the Hydrogen Hypothesis in the article, though it is is referenced in the Endosymbiotic theory article. Can someone please add an appropriate reference?Pmarshal (talk) 06:13, 28 August 2010 (UTC)pmarshal

Parasite Eve[edit]

The book/movie/video game series Parasite Eve centers around a notion that mitochondria is controlled by a single, highly advanced entity, and is largely the basis of the plot. The first game sold over 1 million copies, as well as the second game; perhaps the series could be mentioned in the article. --Chiefmartinez (talk) 05:35, 23 February 2011 (UTC)