Talk:L-DOPA

INN

In accordance with Wikipedia:WikiProject_Drugs naming policy, I propose we move this page to the INN levodopa. If you have any concern with this proposal, please discuss it on this page. Matt 18:09, 23 Dec 2004 (UTC)

Done. -Techelf 12:33, 27 May 2006 (UTC)

Dopamine decarboxylase

Under the Therapeutic Use section, I'm pretty sure that this statement is wrong:

"so it is administered with a peripheral DDC (dopamine decarboxylase) inhibitor such as carbidopa"

I believe that it should be "DOPA decarboxylase" instead of "dopamine decarboxylase"

Could you please address this minor fault.

You're right, the enzyme involved is aromatic L-amino acid decarboxylase (a.k.a. DOPA decarboxylase). Article updated. -Techelf 12:33, 27 May 2006 (UTC)

L-DOPA in food

Could someone please include some information on l-dopa in foods? The fava bean, for example, contains a high level of "natural" l-dopa.

The only foods I've heard of containing L-dopa is Fava beans and Mucuna pruriens (also a type of bean in which you can buy in supplement form). — Preceding unsigned comment added by 24.145.233.62 (talk) 14:14, 20 September 2011 (UTC)

Hypotension

Maybe I'm missing something, but wouldn't L-DOPA, being converted in the periphery to dopamine, therefore cause an increase in blood pressure?-Anodyne 25 September 2006

yes yes please answer this question...i thought dopamine would increase blood pressure...and also even after it gets converted to noradrenaline and adrenaline it would still cause hypertension.... i was just wondering if this is the answer...if theres too much adrenaline in blood it causes the fight flight fright responses...then it would direct the blood to the muscles of the legs so it would help us to run faster (to get out of there)and causes other things like increase heart rate and ilke dilation of pupils (to see better) and etc.... so in an overdose of L-dopa you get too much vasodilation in the muscles and too much vessel constriction in the gut and stuff...and the blood pools away in the muscle causing hypotension inside the organs?

L dopa revives coma victims

As is the premise of the latest episode of House. Why is there no mention of this? It's use of reviving coma victims originated in south africa, its revival only lasts 4 hours. Very interesting, like temporary revival of the dead, just to ask some questions.

House = Fiction. QED. Zerocannon 16:28, 16 October 2007 (UTC)

This not "exactly" fiction, for certain values of exactly.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1344209

Here is a more "pop-sci" article if you do not enjoy medical journels

http://www.timesonline.co.uk/tol/news/uk/article727295.ece

Agalmic (talk) 15:39, 25 May 2008 (UTC)

Levodopa elevates homocysteine

There are articles telling of homocysteine increase due to levodopa, and studies showing that folic acid could help with this. Best regards, CopperKettle 10:18, 20 March 2007 (UTC)

Badly written introductory paragraph ;(

Needs some work. — Preceding unsigned comment added by 24.246.236.191 (talk) 03:57, 28 September 2014 (UTC)

Levodopa and hypotension

Levodopa increases all of the catecholamines, but mostly dopamine. Since dopamine is an adrenergic, you might expect it to cause hypertension, but it is a selective-beta adrenergic receptor agonist with no significant alpha action. Whereas alpha receptors constrict blood vessels in intestines and stomach and stuff, beta receptors dilate vessels in skeletal muscle to allow more nutrients to go to the muscles. The result is that since levodopa mainly increases dopamine, and dopamine works only on beta receptors, blood vessel only dilate and hypotension can occur. —Preceding unsigned comment added by 76.216.99.188 (talk) 06:45, 14 January 2008 (UTC)

Toxicity issues

I have added some information on cellular and neuronal toxicity induced by Levodopa in the "Adverse Effects" section of the article, and have provided references to medical research journals for the statements. I believe, however, that such a section should be enlarged to include more of these related issues, as the drug is sold over the counter as a dietary supplement and safety information (especially from extracts) is scarce.

18:03, 8 March 2008 (UTC)

Article Move

This article should be called L-DOPA. L-DOPA is the common, scientific name for a chemical which exists as a biosynthetic precursor to dopamine and can also be synthesized in the lab. Levadopa is the INN for synthetic L-DOPA intended for use as a pharmaceutical. Since this article is about the substance as a chemical (structure, synthesis, etc.), the natural biological properties (synthesis, function, etc.), and its use as a pharmaceutical (role in Parkinsons, dosing, etc.) we should use the most general name, not the pharmaceutical specific one. --Selket ^Talk 03:34, 25 July 2008 (UTC)

Why the uppercase? Shouldn’t this be spelled “L-dopa”? Palpalpalpal (talk) 00:29, 29 October 2012 (UTC)

Excessively detailled discussion of reserach papers on toxity, moved to talk

Large section added by 69.23.138.116 (talk · contribs) that is either original research ("Our observations") or if not personal commentary then is a copy of text from somewhere else which has not been rephrased for encyclopaedic style - failling this, then a conflict of interest to add one's own material directly into articles without discussion in talk page 1st. See WP:No original research and WP:Conflict of interest.

So here is the added text that we might look at:

---

Several studies show it is not toxic and actually is quite neuroprotective.

Adv Neurol. 2001;86:327-36.L The protective role of levodopa in the human substantia nigra. Rajput AH. Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, S7N 0W8, Canada.

Laboratory studies and studies of animal models of parkinsonism have produced contradictory evidence, but there is no evidence that LD is toxic to normal substantia nigra in animals. We have studied human subjects longitudinally to address that issue. A cumulative LD dose up to 24 kg was not toxic in one autopsied essential tremor (ET) case. Two other ET patients did not develop parkinsonism on 8.5 kg and 21 kg cumulative LD dose, respectively. One DOPA-responsive dystonia (DRD) case has no evidence of parkinsonism after 29 years and more than 17 kg of LD. A DRD patient who received 3 kg over 11 years had normal SN neuronal complement at autopsy. One patient who has clinical and laboratory evidence of nigral pathology as the basis of parkinsonism when untreated for 18 years had progressive disability. While on LD he has excellent symptomatic benefit and virtual cessation of progression of the disease. Epidemiologic studies indicate that those prescribed LD at an early stage of illness and hence given larger cumulative lifetime doses have longer survival than those in whom LD is started late and who receive smaller total doses. Our observations and the available literature support that levodopa is not toxic to normal or diseased substantia nigra in human beings. Evidence presented here indicates that levodopa has a protective effect on the human substantia nigra neurons.

Mov Disord. 1997 Sep;12(5):634-8.L Is levodopa toxic to human substantia nigra?

Rajput AH, Fenton M, Birdi S, Macaulay R. Division of Neurology, Royal University Hospital, Saskatoon, Saskatchewan, Canada.

Levodopa (LD) is the most effective drug for symptomatic control of Parkinson's disease, but has been suspected to be toxic to substantia nigra (SN) dopaminergic neurons. Tissue culture and animal studies of LD toxicity have produced contradictory evidence, and one study reported that a human subject exposed to a large cumulative dose (cd) of LD over 4 years had no evidence of SN damage. We report the cases of five patients, each of whom received a large cd of LD over a long period. Fluorodopa positron-emission tomography performed in one case indicated parkinsonism. Autopsies in two cases indicated a normal SN in one and a hypopigmented SN with normal cell complement in the other. Three patients had essential tremor, one had nonprogressive parkinsonism, and one had dopa-responsive dystonia. LD (without decarboxylase inhibitor) was administered over 21 years (cd = 21.99 kg), 9 years (cd = 6.6 kg), 26 years (cd = 18.7 kg), 11 years (cd = 3 kg), and 26 years (cd = 23.93 kg), respectively. None of the patients with essential tremor developed clinical features of parkinsonism that indicated significant SN damage, and one had a normal SN at autopsy. The parkinsonian patient displayed no detectable acceleration of disease process, and the patient with dopa-responsive dystonia had a normal complement of SN neurons at autopsy. We conclude that LD, administered at a dose commonly used for treating Parkinson's disease, was not toxic to SN neurons in these cases.

Parkinsonism Relat Disord. 2001 Oct;8(2):95-100. Levodopa prolongs life expectancy and is non-toxic to substantia nigra.

Rajput AH.Neurology Division, Royal University Hospital, 103 Hospital Drive, Saskatoon, SK, Canada S7N 0W8. rajputa@sdh.sk.ca

The primary objective of the study was to determine the effect of levodopa (LD) on human substantia nigra. The study included patients seen at the Movement Disorder Clinic, Saskatoon over a 32 year period. The evidence provided is based on epidemiological observations of 934 consecutive Parkinson syndrome (PS) patients assessed during 22 years and detailed studies of six patients including two autopsies. Life expectancy increased significantly with LD therapy. The prolonged survival was evident when the patients were treated during early stage of the illness. One parkinsonian patient with substantia nigra (SN) pathology who was extensively studied for 30 years, revealed significant slowing of the disease progression while on LD. Three essential tremor patients who received 24 kg (26 years), 22 kg (21.5 years), and 8.5 kg (12.5 years) LD respectively, had no evidence of PS and one autopsy revealed normal SN. Two dopa-responsive dystonia patients who received LD 3 kg (11 years) and 17 kg (29 years) each had no evidence of PS and one autopsy revealed normal number of SN neurons.These observations indicate that LD is not toxic to human SN and are consistent with salutary effect of the drug on the SN in Parkinson's disease.

Mov Disord. 2001 May;16(3):424-34.L Chronic L-DOPA administration is not toxic to the remaining dopaminergic nigrostriatal neurons, but instead may promote their functional recovery, in rats with partial 6-OHDA or FeCl(3) nigrostriatal lesions.

Datla KP, Blunt SB, Dexter DT. Parkinson's Disease Research Unit, Department of Neuroinflammation, Imperial College School of Medicine at Charing Cross Campus, Fulham Palace Road, London W6 8RF, United Kingdom.

In this study, we have examined the effects of chronic L-3,4-dihydroxyphenylalanine (L-DOPA) administration on the remaining dopaminergic neurons in rats with 6-hydroxydopamine (6-OHDA) or buffered FeCl(3) partial lesions to the nigrostriatal tract. L-DOPA administration increased the turnover of dopamine in the striatum. L-DOPA administration for 1 week produced an increase in the level of striatal RTI-121 binding, a specific marker for dopamine uptake sites on the dopaminergic nerve terminals in the striatum. However, longer periods of L-DOPA treatment decreased the level of RTI-121 binding in the striatum. In the partial 6-OHDA lesion model, L-DOPA treatment had a time-dependent effect on the number of neurons demonstrating a dopaminergic phenotype i.e., neurons that are tyrosine hyrdoxylase (TH)-immunopositive, on the lesioned side of the brain. In the first few weeks of treatment, L-DOPA decreased the number of TH-positive neurons but with long-term treatment, i.e., 24 weeks, L-DOPA increased the number of neurons demonstrating a dopaminergic phenotype. Even in the buffered FeCl(3) infusion model, where the levels of iron were increased, L-DOPA treatment did not have any detrimental effects on the number of TH-positive neurons on the lesioned side of the brain. Consequently, chronic L-DOPA treatment does not have any detrimental effects to the remaining dopaminergic neurons in rats with partial lesions to the nigrostriatal tract; indeed in the 6-OHDA lesion model, long-term L-DOPA may increase the number of neurons, demonstrating a dopaminergic phenotype.

J Neurochem. 1996 Feb;66(2):501-10. L-DOPA up-regulates glutathione and protects mesencephalic cultures against oxidative stress.

---

Irrespective of the value of the studies mentioned, wikipedia does not generally give abstracts of studies, rather it states a fact or opinion and then cites the source, allowing readers to go and look at the details (providing PubMed links will allow linkage online to the abstracts) David Ruben ^Talk 00:52, 3 September 2008 (UTC)

As a start, the above seems to cite 5 papers, here are the full references marked up using {{cite journal}} template (view edit screen to view the markup that may be later copied into any article text), and providing PubMed PMID and doi links to abstracts we can read:

• Rajput AH (2001). "The protective role of levodopa in the human substantia nigra". Adv Neurol. 86: 327–36. PMID 11553992.
• Rajput AH, Fenton M, Birdi S, Macaulay R (1997). "Is levodopa toxic to human substantia nigra?". Mov. Disord. 12 (5): 634–8. doi:10.1002/mds.870120503. PMID 9380042. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
• Rajput AH (2001). "Levodopa prolongs life expectancy and is non-toxic to substantia nigra". Parkinsonism Relat. Disord. 8 (2): 95–100. PMID 11489674. {{cite journal}}: Unknown parameter |month= ignored (help)
• Datla KP, Blunt SB, Dexter DT (2001). "Chronic L-DOPA administration is not toxic to the remaining dopaminergic nigrostriatal neurons, but instead may promote their functional recovery, in rats with partial 6-OHDA or FeCl(3) nigrostriatal lesions". Mov. Disord. 16 (3): 424–34. PMID 11391735. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
• Han SK, Mytilineou C, Cohen G (1996). "L-DOPA up-regulates glutathione and protects mesencephalic cultures against oxidative stress". J. Neurochem. 66 (2): 501–10. PMID 8592119. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

David Ruben ^Talk 01:10, 3 September 2008 (UTC)

Jytdog (talk) 23:22, 26 August 2009 (UTC)moved the paragraph on "Epigallocatechin gallate" from Drugs to Dietary Supplements, as Epigallocatechin gallate is not a drug. This is some academic research and we don't want people thinking Epigallocatechin gallate is a drug.

Side Effects: Disturbed respiration

Under side effects it states: "Disturbed respiration, which is not always harmful, and can actually benefit patients with upper airway obstruction"

This is somewhat counter-intuitive and contrary to basic emergency medicine. I would like citation, clarification, or removal. It is possible that this is simply a miscomunication and would benifit from a better explination/clarifiction (Croaker260 (talk) 20:22, 27 February 2012 (UTC))

As a nootropic

"...lighter people from the drug group did better than the non-light people.[21]"

I don't have access to the reference, so what are "lighter" and "non-light" people? Lighter body mass? Highly pigmented skin? EdwardEditor (talk) 01:21, 27 September 2014 (UTC)

movie

L-Dopa was the mirical drug that was the basis for the book and movie Awakenings. Herogamer (talk) 18:16, 19 March 2012 (UTC)

Unused references

The following were appended to the references section, but are currently not used to support any specific article content as far as I can tell. I'm moving them here in case anyone would like to use them to expand the article. -- Ed (Edgar181) 13:08, 1 May 2012 (UTC)

• Waite; J. Herbert; et al. (2005). "Mussel Adhesion: Finding the Tricks Worth Mimicking". J Adhesion. 81 (3–4): 1–21. doi:10.1080/00218460590944602. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
• Messersmith; Phillip B.; et al. (2006). "Rapid Gel Formation and Adhesion in Photocurable and Biodegradable Block Copolymers with High DOPA Content". Macromolecules. 39 (5): 1740–1748. doi:10.1021/ma0518959. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
• " The Diagnostics and Theraphy of Incurable Nervous and Psychic Diseases of Dopamine Etiology. Biocorrection Method by Prof.V.Vasiliev ", author: Prof.Vitaly N.Vasiliev, Moscow: Mediakit Publishing , 2011,- 294 pages

@Edgar181: Unless you are certain there is no content in the article from those sources (which would be quite a feat), they should remain in the article, even though they are not cited with inline citations. It's not ideal to cite this way, but it's still better than not citing at all. I've added them back again. —[AlanM1(talk)]— 00:51, 30 September 2013 (UTC)

Looking closely at the article and those references, I moved one inline and removed two as unrelated to any current article content. I also moved the external link into the article as a reference because it supported article content. -- Ed (Edgar181) 13:02, 30 September 2013 (UTC)

Small L in name?

Why is the leading "L" in the name small (i.e. L-DOPA)? Should this be worked into the article? —[AlanM1(talk)]— 00:59, 30 September 2013 (UTC)

It is a chemical nomenclature convention to use small caps font for D/L nomenclature. IMHO, this is trivia that is out of the scope of this article. -- Ed (Edgar181) 13:07, 30 September 2013 (UTC)

Neurotransmitter depletion

So under the side effects section, possible neurotransmitter depletion was placed there, without a citation.

I found a paper in the literature (5-HTP efficacy and contraindications), but the ideas seem sketchy to me. While competitive inhibition is certainly possible, they repeatedly cite themselves, and many of their previous papers appear to be bordering on what is colloquially called "bro-science" - unsubstantiated and often dramatic claims, or poor quality experiments/studies. Could someone else please take a look at this source and verify its credibility? (Erebusthedark (talk) 23:46, 5 March 2014 (UTC))

permanent effects/ effect in non parkinsonian people?

is there any knowledge regarding what are the consequences of quitting (withdrawal symptomes of) the L-Dopa, or about it's effects (and if there are any, then how transient/permanent they are) on people/lab animal models without parkinson's disease (or parkinsonian symptomes inflicted by other causes)?176.63.176.112 (talk) 20:50, 28 February 2017 (UTC)

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Dopamine functions as a neurotransmitter outside the CNS

Seppi333, while it is correct that dopamine can be classified as a hormone due to the characteristics of some of its physiological effects on homeostasis outside of the CNS, it nevertheless functions as a neurotransmitter. Also; "peripheral dopmanine" carries no meaning what so ever, the molecule is non-chiral. As the primary negative effects of sole administration of L-DOPA stems from dopamine in its role as a neurotransmitter, I thought it less relevant to also mention dopamine's role as a hormone. Your edit carried some less relevant correction, but still worthy of a mention. I would claim though, for the most part, your edit made the article less factual. --Rettetasten (talk) 00:54, 3 December 2018 (UTC)

--Rettetasten (talk) 00:49, 3 December 2018 (UTC)

@Rettetasten: Outside the CNS, DA gets around and binds to its receptor targets via the blood stream (i.e., it functions as a hormone outside the brain). Inside the brain, it’s primarily released from DA neurons onto their target neurons that express DA receptors (i.e., it largely functions as a neurotransmitter inside the brain). That’s not a trivial distinction. If you happen to know of neurons that release dopamine onto other neurons in the peripheral nervous system, I would be interested in reading the corresponding literature, and we should definitely cover that. I’m not aware of any literature that mentions the existence of any peripheral DA neurons, however. Seppi333 (Insert 2¢) 17:30, 3 December 2018 (UTC)

@Seppi333: I'll just start simple, just to give you an idea of where I'm going. From https://www.britannica.com/science/neurotransmitter: "Neurotransmitters are synthesized by neurons and are stored in vesicles, which typically are located in the axon’s terminal end, also known as the presynaptic terminal. The presynaptic terminal is separated from the neuron or muscle or gland cell onto which it impinges by a gap called the synaptic cleft. The synaptic cleft, presynaptic terminal, and receiving dendrite of the next cell together form a junction known as the synapse." Note the part i put in italic. I hope this will at least motivate you to dig a bit deeper on your own. Should it in the end come to it, I guess I'm going to have to resort to https://www.ncbi.nlm.nih.gov/pubmed/ That takes alot of time however, and should be unnecessary. Perhaps a Third opinion (3O) would be the best way to go? Edit: Just wanted to add the "good faith"-tag. But contributing to Wikipedia is becoming more and more like writing assembly, with instructions only provided in a yet to be deciphered language read backwards. Rettetasten (talk) 21:52, 5 December 2018 (UTC)

My point is that the PNS uses norepinephrine and acetylcholine, not dopamine. Neuromuscular junctions in particular are innervated solely by acetylcholine (motor) neurons. A 3O isn't appropriate when uncited content is removed from an article. If what you say is true, it still needs to be cited per WP:V. If it isn't, stating it in an article constitutes WP:OR. Lastly, if we say "dopamine is a neurotransmitter in the PNS" without specifying where, we'd be writing a shitty encyclopedia article. Seppi333 (Insert 2¢) 23:37, 5 December 2018 (UTC)

Fair enough. I have no qualms regarding the need for citations. Seeing as you were the one to quite confidently claim dopamine is not to be concidered a neurotransmitter outside the CNS, I dare claim it rests on your shoulders to provide said citations, taking for granted the paragraph I edited was already in lack of citations. In the case you should not find the time to find appropriate citations, I recon the only fair thing, would be for you to revert the article to my last edit. Else, I see no other option than to request a 3O, or any other similar third party review. Rettetasten (talk) 00:05, 6 December 2018 (UTC)

With rare exception, one can almost never find a negative statement like that (i.e., X is not Y) in a reliable source; that should be obvious because "Y" in that example statement is typically an infinite number of things. In other words, I doubt I'd find a source that explicitly states "DA is not a neurotransmitter in the PNS." However, it would not be hard to find what neurotransmitters are used in the PNS.

That said, we already include content on dopamine in the periphery in this article: Dopamine#Outside the nervous system. Seppi333 (Insert 2¢) 00:52, 6 December 2018 (UTC)

3O Response: The only citations in that paragraph are for the brand-name drugs and the sources don't appear to cover the contested material. It seems as though the first sentences of related article Dopamine § Outside the nervous system have offline sources that could be used here, if either of you have access to them. I tend to prefer Rettetasten's wording, though as a compromise I might use the words Dopamine's role[s] as a neurotransmitter in the two systems are not mutually comparable with those struck-out removed, if that would be more agreeable. I would also note that as a copy editor, I like to see peripheral nervous system (PNS) and then PNS thereafter instead of "periphery", unless that has a different intended meaning. – Reidgreg (talk) 20:39, 7 December 2018 (UTC)