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==Increasing maximum life span==
==Increasing maximum life span==
Currently, the only (non-[[Genetically modified organisms|transgenic]]) method of increasing maximum life span that is recognized by [[Gerontology|biogerontologists]] is [[calorie restriction]] with adequate nutrition. However, this is true only if we use definition 2 of maximum life span, as caloric restriction has not yet been shown to break mammalian world records for longevity. [[Rat]]s, [[mouse|mice]] and [[hamster]]s experience maximum life span extension from a diet which contains 40−60% of the calories (but all of the required nutrients) which the animals consume when they can eat as much as they want. [[Mean life span]] is increased 65% and maximum life span is increased 50%, when calorie restriction is begun just before [[puberty]]. (For a recent review of maximum lifes span extension by calorie restriction in rodent studies, see [http://www.genesdev.org/cgi/content/full/17/3/313 GENES & DEVELOPMENT; Koubova,J; 17(3):313-321 (2003)]). For [[fruit flies]] the life extending benefits of calorie restriction are gained immediately at any age upon beginning calorie restriction and ended immediately at any age upon resuming full feeding [ [[Science (journal)|SCIENCE]]; Mair,W; 301:1731-1733 (2003) ].
Currently, the only (non-[[Genetically modified organisms|transgenic]]) method of increasing maximum life span that is recognized by [[Gerontology|biogerontologists]] is [[calorie restriction]] with adequate nutrition. However, this is true only if we use definition 2 of maximum life span, as caloric restriction has not yet been shown to break mammalian world records for longevity. [[Rat]]s, [[mouse|mice]] and [[hamster]]s experience maximum life span extension from a diet which contains 40&minus;60&#37; of the calories (but all of the required nutrients) which the animals consume when they can eat as much as they want. [[Mean life span]] is increased 65&#37; and maximum life span is increased 50&#37;, when calorie restriction is begun just before [[puberty]]. (For a recent review of maximum lifes span extension by calorie restriction in rodent studies, see [ GENES & DEVELOPMENT; Koubova,J; 17(3):313-321 (2003)] <ref>{{cite journal | author=Koubova J, Guarente L. | title=How does calorie restriction work? | journal=GENES & DEVELOPMENT | volume=17 | issue=3 | year=2003 | pages=313-321 | url=http://www.genesdev.org/cgi/content/full/17/3/313 |id=PMID 12569120 }}</ref>). For [[fruit flies]] the life extending benefits of calorie restriction are gained immediately at any age upon beginning calorie restriction and ended immediately at any age upon resuming full feeding [ [[Science (journal)|SCIENCE]]; Mair,W; 301:1731-1733 (2003) <ref>{{cite journal | author=Mair W, Goymer P, Pletcher SD, Partridge L. | title=Demography of dietary restriction and death in Drosophila | journal=[[Science (journal)|SCIENCE]] | volume=301 | issue=5640 | year=2003 | pages=1731-1733 | id=PMID 114500985 }}</ref> ].


Mammals fed [[anti-oxidant]]s show up to a 30&#37; increase in [[mean life span]], but no increase in maximum life span. [[Antioxidants]] are most valuable for animals that are cancer-prone, or subjected to [[radiation]] or [[chemical]] toxins. There are evidently homeostatic mechanisms in cells that govern the amount of allowable antioxidant activity. Many [[Life extension|life-extensionists]] have dismissed the value of antioxidants simply because they have not been shown to increase maximum life span -- as if extending [[mean life span]] was not important.
Mammals fed [[anti-oxidant]]s show up to a 30&#37; increase in [[mean life span]], but no increase in maximum life span. [[Antioxidants]] are most valuable for animals that are cancer-prone, or subjected to [[radiation]] or [[chemical]] toxins. There are evidently homeostatic mechanisms in cells that govern the amount of allowable antioxidant activity. Many [[Life extension|life-extensionists]] have dismissed the value of antioxidants simply because they have not been shown to increase maximum life span -- as if extending [[mean life span]] was not important.
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==Research data concerning maximum life span==
==Research data concerning maximum life span==
* A comparison of the [[heart]] [[mitochondria]] in rats (4-year maximum life span) and [[pigeon]]s (35-year maximum life span) showed that pigeon [[mitochondria]] leak fewer [[radical (chemistry)|free-radicals]] than rat mitochondria, despite the fact that both animals have similar [[metabolic rate]] and [[cardiac]] output
* A comparison of the [[heart]] [[mitochondria]] in rats (4-year maximum life span) and [[pigeon]]s (35-year maximum life span) showed that pigeon [[mitochondria]] leak fewer [[radical (chemistry)|free-radicals]] than rat mitochondria, despite the fact that both animals have similar [[metabolic rate]] and [[cardiac]] output <ref>{{cite journal | author=Herrero A, Barja G. | title=Sites and mechanisms responsible for the low rate of free radical production of heart mitochondria in the long-lived pigeon | journal=MECHANISMS OF AGING AND DEVELOPMENT | volume=98 | issue=2 | year=1997 | pages=95-111 | id=PMID 9379714 }}</ref>
::[MECHANISMS OF AGING AND DEVELOPMENT 98:95-111 (1997)]


* For [[mammal]]s there is a direct relationship between [[mitochondria]]l [[membrane]] saturation and maximum life span
* For [[mammal]]s there is a direct relationship between [[mitochondria]]l [[membrane]] saturation and maximum life span <ref>{{cite journal | author=Pamplona R, Portero-Otin M, Riba D, Ruiz C, Prat J, Bellmunt MJ, Barja G. | title=Mitochondrial membrane peroxidizability index is inversely related to maximum life span in mammals | journal=JOURNAL OF LIPID RESEARCH | volume=39 | issue=2 | year=1998 | pages=1989-1994 | url=http://www.jlr.org/cgi/content/full/39/10/1989 | id=PMID 9788245 }}</ref>
::[JOURNAL OF LIPID RESEARCH 39:1989-1994 (1998)]


* Studies of the [[liver]] [[lipid]]s of [[mammal]]s and a [[bird]] ([[pigeon]]) show an inverse relationship between maximum life span and number of [[double bond]]s
* Studies of the [[liver]] [[lipid]]s of [[mammal]]s and a [[bird]] ([[pigeon]]) show an inverse relationship between maximum life span and number of [[double bond]]s <ref>{{cite journal | author=Pamplona R, Portero-Otin M, Riba D, Requena JR, Thorpe SR, Lopez-Torres M, Barja G. | title=Low fatty acid unsaturation: a mechanism for lowered lipoperoxidative modification of tissue proteins in mammalian species with long life spans | journal=JOURNALS OF GERONTOLOGY SERIES&nbsp;A BIOLOGICAL SCIENCES AND MEDICAL SCIENCES | volume=55A | issue=6 | year=2000 | pages=B286-B291 | id=PMID 10843345 }}</ref>
::[JOURNAL OF GERONTOLOGY 55A(6):B286-B291 (2000)]


* Maximum life span correlates negatively with [[antioxidant]] [[enzyme]] levels and correlates positively with lower rate of [[radical (chemistry)|free-radicals]] production and higher rate of [[DNA repair]]
* Maximum life span correlates negatively with [[antioxidant]] [[enzyme]] levels and correlates positively with lower rate of [[radical (chemistry)|free-radicals]] production and higher rate of [[DNA repair]] <ref>{{cite journal | author=Perez-Campo R, Lopez-Torres M, Cadenas S, Rojas C, Barja G. | title=The rate of free radical production as a determinant of the rate of aging: evidence from the comparative approach. | journal=JOURNAL OF COMPARATIVE PHYSIOLOGY. B, Biochemical, systemic, and environmental physiology | volume=168 | issue=3 | year=1998 | pages=149-158 | id=PMID 9591361 }}</ref>
::[JOURNAL OF COMPARATIVE PHYSIOLOGY&nbsp;B 168:149-158 (1998)]


* Females express both more Mn&minus;SOD and more glutathione peroxidase antioxidant [[enzyme]]s than males, and this has been suggested to be the reason females live longer than males in [[mammal]]ian species
* Females express both more Mn&minus;SOD and more glutathione peroxidase antioxidant [[enzyme]]s than males, and this has been suggested to be the reason females live longer than males in [[mammal]]ian species <ref>{{cite journal | author=Vina J, Borras C, Gambini J, Sastre J, Pallardo FV. | title=Why females live longer than males? Importance of the upregulation of longevity-associated genes by oestrogenic compounds | journal=FEBS LETTERS | volume=579 | issue=12 | year=2005 | pages=2541-2545 | id=PMID 15862287 }}</ref>
::[FEBS LETTERS; Vina,J; 579(12):2541-2545 (2005)]


* The maximum life span of transgenic mice has been extended about 20&#37; by overexpression of human [[catalase]] targeted to [[mitochondria]]
* The maximum life span of transgenic mice has been extended about 20&#37; by overexpression of human [[catalase]] targeted to [[mitochondria]] <ref>{{cite journal | author=Schriner SE, Linford NJ, Martin GM, Treuting P, Ogburn CE, Emond M, Coskun PE, Ladiges W, Wolf N, Van Remmen H, Wallace DC, Rabinovitch PS. | title=Extension of murine life span by overexpression of catalase targeted to mitochondria | journal=[[Science (journal)|SCIENCE]] | volume=308 | issue=5730 | year=2005 | pages=1909-1911 | id=PMID 15879174 }}</ref>
::[ [[Science (journal)|SCIENCE]]; Schriner,SE; 308:1909-1911 (2005)]


* A comparison of 7 non-[[primate]] [[mammal]]s (mouse, hamster, rat, guinea-pig, rabbit, pig and cow) showed that the rate of [[mitochondrial]] superoxide and hydrogen peroxide production in [[heart]] and [[kidney]] were inversely correlated with maximum life span
* A comparison of 7 non-[[primate]] [[mammal]]s (mouse, hamster, rat, guinea-pig, rabbit, pig and cow) showed that the rate of [[mitochondrial]] superoxide and hydrogen peroxide production in [[heart]] and [[kidney]] were inversely correlated with maximum life span <ref>{{cite journal | author=Ku HH, Brunk UT, Sohal RS. | title=Relationship between mitochondrial superoxide and hydrogen peroxide production and longevity of mammalian species | journal=FREE RADICAL BIOLOGY &amp; MEDICINE | volume=15 | issue=6 | year=1993 | pages=621-627 | id=PMID 8138188 }}</ref>
::[FREE RADICAL BIOLOGY &amp; MEDICINE 15:621-627 (1993)]


* A study of 8 non-[[primate]] [[mammals]] showed a direct correlation between maximum life span and oxidative damage to mtDNA ([[mitochondria|mitochondrial]] [[DNA]]) in heart &amp; brain
* A study of 8 non-[[primate]] [[mammals]] showed a direct correlation between maximum life span and oxidative damage to mtDNA ([[mitochondria|mitochondrial]] [[DNA]]) in heart &amp; brain <ref>{{cite journal | author=Barja G, Herrero A. | title=Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heart and brain of mammals | journal=THE FASEB JOURNAL | volume=14 | issue=2 | year=2000 | pages=312-318 | url=http://www.fasebj.org/cgi/content/full/14/2/312 | id=PMID 10657987 }}</ref>
::[THE FASEB JOURNAL; Barja,G; 14(2):312-318 (2000)]


* A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span
* A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span <ref>{{cite journal | author=Agarwal S, Sohal RS. | title=Relationship between susceptibility to protein oxidation, aging, and maximum life span potential of different species | journal=EXPERIMENTAL GERONTOLOGY | volume=31 | issue=3 | year=1996 | pages=365-372 | id=PMID 9415119 }}</ref>
::[EXPERIMENTAL GERONTOLOGY 31(3):387-392 (1996)]


* There is a direct correlation between [[DNA repair]] and maximum life span for [[mammal]]ian species
* There is a direct correlation between [[DNA repair]] and maximum life span for [[mammal]]ian species <ref>{{cite journal | author=Cortopassi GA, Wang E. | title=There is substantial agreement among interspecies estimates of DNA repair activity | journal=MECHANISMS OF AGING AND DEVELOPMENT | volume=91 | issue=3 | year=1996 | pages=211-218 | id=PMID 9055244 }}</ref>
::[MECHANISMS OF AGING AND DEVELOPMENT; Cortopassi, GA; 91:211-218 (1996)]


* [[Drosophila]] (fruit-flies) bred for 15&nbsp;generations by only using eggs that were laid toward the end of reproductive life achieved maximum life spans 30&#37; greater than that of controls
* [[Drosophila]] (fruit-flies) bred for 15&nbsp;generations by only using eggs that were laid toward the end of reproductive life achieved maximum life spans 30&#37; greater than that of controls <ref>{{cite journal | author=Kurapati R, Passananti HB, Rose MR, Tower J. | title=Increased hsp22 RNA levels in Drosophila lines genetically selected for increased longevity | journal=JOURNALS OF GERONTOLOGY SERIES&nbsp;A BIOLOGICAL SCIENCES AND MEDICAL SCIENCES | volume=55A | issue=11 | year=2000 | pages=B552-B559 | id=PMID 11078089 }}</ref>
::[JOURNALS OF GERONTOLOGY 55A(11):B552-B559 (2000)]


* A mutation in the <B>age&minus;1</B> gene of the [[nematode]] [[worm]] [[Caenorhabditis elegans]] inceased [[mean life span]] 65&#37; and maximum life span 110&#37;
* A mutation in the <B>age&minus;1</B> gene of the [[nematode]] [[worm]] [[Caenorhabditis elegans]] inceased [[mean life span]] 65&#37; and maximum life span 110&#37; <ref>{{cite journal | author=Friedman DB, Johnson TE. | title=A mutation in the age-1 gene in Caenorhabditis elegans lengthens life and reduces hermaphrodite fertility | journal=GENETICS | volume=118 | issue=1 | year=1988 | pages=75-86 | url=http://www.genetics.org/cgi/reprint/118/1/75 | id=PMID 8608934}}</ref>
::[GENETICS 118:75-86 (1988)]


* [[Fat]]-specific [[Insulin]] [[receptor (biology)|Receptor]] [[Gene knockout|KnockOut]] (<B>FIRKO</B>) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18&#37;
* [[Fat]]-specific [[Insulin]] [[receptor (biology)|Receptor]] [[Gene knockout|KnockOut]] (<B>FIRKO</B>) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18&#37; <ref>{{cite journal | author=Bluher M, Kahn BB, Kahn CR. | title=Extended longevity in mice lacking the insulin receptor in adipose tissue | journal=[[Science (journal)|SCIENCE]] | volume=299 | issue=5606 | year=2003 | pages=572-574 | id=PMID 12543978 }}</ref>
::[ [[Science (journal)|SCIENCE]]; Bluher,M; 299:572-574 (2003)]


* The capacity of mammalian species to detoxify the [[carcinogenic]] chemical benzo(a)pyrene to a water-soluble form also correlates well with maximum life span
* The capacity of mammalian species to detoxify the [[carcinogenic]] chemical benzo(a)pyrene to a water-soluble form also correlates well with maximum life span <ref>{{cite journal | author=Moore CJ, Schwartz AG. | title=Inverse correlation between species lifespan and capacity of cultured fibroblasts to convert benzo(a)pyrene to water-soluble metabolites | journal=EXPERIMENTAL CELL RESEARCH | volume=116 | issue=2 | year=1978 | pages=359-364 | id=PMID 101383 }}</ref>
::[EXPERIMENTAL CELL RESEARCH 116:359-364 (1978)]


== Publications discussing the concept of maximum life span ==
== Publications discussing the concept of maximum life span ==
Line 73: Line 59:
* Gavrilov, L.A., Gavrilova, N.S. Common sense and the limits to life. Int. J. Geriatric Psychiatry, 1993, 8(8): 695-695.
* Gavrilov, L.A., Gavrilova, N.S. Common sense and the limits to life. Int. J. Geriatric Psychiatry, 1993, 8(8): 695-695.
* Gavrilov L.A. Does a limit of the life span really exist? Biophysics [Biofizika], 1984, 29(5): 908-911. PMID 6509106
* Gavrilov L.A. Does a limit of the life span really exist? Biophysics [Biofizika], 1984, 29(5): 908-911. PMID 6509106

==References==
<references/>


==See also==
==See also==

Revision as of 06:24, 12 May 2006

You must add a |reason= parameter to this Cleanup template – replace it with {{Cleanup|April 2006|reason=<Fill reason here>}}, or remove the Cleanup template.
 Maximum life span is a measure of the maximum number of years a member of a group has been observed to survive. Maximum life span literally corresponds to the age at which the oldest known member of a species or experimental group has died. Maximum life span is contrasted to mean life span (average lifespan or life expectancy). Mean life span varies with susceptibility to disease, accident, suicide and homicide, whereas maximum life span is determined by "rate of aging". Epistemologically maximum life span also depends upon initial sample size.[1] In animal studies, maximum life span is typically taken to be the mean life span of the most long-lived 10% of a given cohort. This may be taken to be "definition 2" of 'maximum life span.'

Overview

In ancient Rome average life span was 22 years, but by the mid−1800s the typical North American lived to be 40. Today, people in the most developed countries have an average life span of about 80. Reduction of infant mortality has accounted for most of the increased longevity, but since the 1960s mortality rates among those over 80 years has been decreasing by about 1.5% per year. Maximum life span for humans, however, has remained about 115−120 all through known history. The oldest-ever person was Jeanne Calment, a French woman who lived for 122 years and 164 days.

Advances in medicine, calorie restriction with adequate nutrition, or other interventions are said to have slowed the aging process.

The maximum life span of each species is different. These differences demonstrate the role of genetics in determining maximum life span ("rate of aging"). For goldfish, the record is 49; for mice, 4; for dogs, 29; for cats, 34; for horses, 62; for elephants, 78; for humans, 122. The longest-lived animals have been variously described as whales (about 210 years) and tortoises (255 years). Although considered fiction for a time, recent research has indicated that bowhead whales recently killed still had harpoons in their bodies from the 1790's, which, along with analysis of amino acids, has indicated a maximum life span so far of 211 years [2]. Birds and squirrels rarely live to their maximum life span, usually dying of accidents and disease. Grazing animals show wear-and-tear to their teeth to the point where they can no longer eat, and they die of starvation.

The maximum life span of most species has not been accurately determined because the data collection has been minimal and the number of species studied in captivity (or by monitoring in the wild) has been small. Maximum life span is usually longer for species that are larger, can fly and have larger brains. Of the approximately 30,000 genes in the human genome, it is estimated that only 2% of these are different from those of a chimpanzee, which has half the estimated maximum life span of a human. The difference in longevity could be due to as few as a hundred genes or less, however there may be other factors which influence the life span of chimpanzees.

Identical twins tend to die within 3 years of each other, whereas fraternal twins tend to die within 6 years. Aging theories associated with DNA include programmed aging (or programmed aging-resistance) and theories that link aging with DNA damage/mutation or DNA repair capability.

Plants tend to come in annuals, biennials, and perennials. The longer-lived perennials, woody-stemmed plants such as trees and bushes, often live for hundreds and even thousands of years. The oldest-known tree is the bristlecone pine, at 4700 years; it has been claimed that creosote bushes live for 11,000 years, but claims of this nature are based on estimates, rather than actual ring counts.

Increasing maximum life span

Currently, the only (non-transgenic) method of increasing maximum life span that is recognized by biogerontologists is calorie restriction with adequate nutrition. However, this is true only if we use definition 2 of maximum life span, as caloric restriction has not yet been shown to break mammalian world records for longevity. Rats, mice and hamsters experience maximum life span extension from a diet which contains 40−60% of the calories (but all of the required nutrients) which the animals consume when they can eat as much as they want. Mean life span is increased 65% and maximum life span is increased 50%, when calorie restriction is begun just before puberty. (For a recent review of maximum lifes span extension by calorie restriction in rodent studies, see [ GENES & DEVELOPMENT; Koubova,J; 17(3):313-321 (2003)] [1]). For fruit flies the life extending benefits of calorie restriction are gained immediately at any age upon beginning calorie restriction and ended immediately at any age upon resuming full feeding [ SCIENCE; Mair,W; 301:1731-1733 (2003) [2] ].

Mammals fed anti-oxidants show up to a 30% increase in mean life span, but no increase in maximum life span. Antioxidants are most valuable for animals that are cancer-prone, or subjected to radiation or chemical toxins. There are evidently homeostatic mechanisms in cells that govern the amount of allowable antioxidant activity. Many life-extensionists have dismissed the value of antioxidants simply because they have not been shown to increase maximum life span -- as if extending mean life span was not important.

Many transgenic species of mice have been created which have maximum life span greater than that of wild-type or laboratory mice, including Ames dwarf mice, Snell dwarf mice, mice with increased mitochondrial catalase, etc.

Some biomedical gerontologists (the kind of gerontologists who search for ways to extend maximum life span) believe that biomedical molecular engineering can someday extend maximum lifespan and even bring about rejuvenation.

One such researcher is Aubrey de Grey, who calls his project to reverse the damage we call aging SENS (Strategies for Engineered Negligible Senescence). Dr. de Grey has established the The Methuselah Mouse Prize to award money to researchers who can extend the maximum life span of mice.

Research data concerning maximum life span

  • Females express both more Mn−SOD and more glutathione peroxidase antioxidant enzymes than males, and this has been suggested to be the reason females live longer than males in mammalian species [7]
  • The maximum life span of transgenic mice has been extended about 20% by overexpression of human catalase targeted to mitochondria [8]
  • A comparison of 7 non-primate mammals (mouse, hamster, rat, guinea-pig, rabbit, pig and cow) showed that the rate of mitochondrial superoxide and hydrogen peroxide production in heart and kidney were inversely correlated with maximum life span [9]
  • A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span [11]
  • Drosophila (fruit-flies) bred for 15 generations by only using eggs that were laid toward the end of reproductive life achieved maximum life spans 30% greater than that of controls [13]
  • The capacity of mammalian species to detoxify the carcinogenic chemical benzo(a)pyrene to a water-soluble form also correlates well with maximum life span [16]

Publications discussing the concept of maximum life span

  • 1.^ Leonid A. Gavrilov & Natalia S. Gavrilova (1991), The Biology of Life Span: A Quantitative Approach. New York: Harwood Academic Publisher, ISBN 3718649837
  • Gavrilov, L.A., Gavrilova, N.S. Common sense and the limits to life. Int. J. Geriatric Psychiatry, 1993, 8(8): 695-695.
  • Gavrilov L.A. Does a limit of the life span really exist? Biophysics [Biofizika], 1984, 29(5): 908-911. PMID 6509106

References

  1. ^ Koubova J, Guarente L. (2003). "How does calorie restriction work?". GENES & DEVELOPMENT. 17 (3): 313–321. PMID 12569120.
  2. ^ Mair W, Goymer P, Pletcher SD, Partridge L. (2003). "Demography of dietary restriction and death in Drosophila". SCIENCE. 301 (5640): 1731–1733. PMID 114500985.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Herrero A, Barja G. (1997). "Sites and mechanisms responsible for the low rate of free radical production of heart mitochondria in the long-lived pigeon". MECHANISMS OF AGING AND DEVELOPMENT. 98 (2): 95–111. PMID 9379714.
  4. ^ Pamplona R, Portero-Otin M, Riba D, Ruiz C, Prat J, Bellmunt MJ, Barja G. (1998). "Mitochondrial membrane peroxidizability index is inversely related to maximum life span in mammals". JOURNAL OF LIPID RESEARCH. 39 (2): 1989–1994. PMID 9788245.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Pamplona R, Portero-Otin M, Riba D, Requena JR, Thorpe SR, Lopez-Torres M, Barja G. (2000). "Low fatty acid unsaturation: a mechanism for lowered lipoperoxidative modification of tissue proteins in mammalian species with long life spans". JOURNALS OF GERONTOLOGY SERIES A BIOLOGICAL SCIENCES AND MEDICAL SCIENCES. 55A (6): B286–B291. PMID 10843345.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ Perez-Campo R, Lopez-Torres M, Cadenas S, Rojas C, Barja G. (1998). "The rate of free radical production as a determinant of the rate of aging: evidence from the comparative approach". JOURNAL OF COMPARATIVE PHYSIOLOGY. B, Biochemical, systemic, and environmental physiology. 168 (3): 149–158. PMID 9591361.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ Vina J, Borras C, Gambini J, Sastre J, Pallardo FV. (2005). "Why females live longer than males? Importance of the upregulation of longevity-associated genes by oestrogenic compounds". FEBS LETTERS. 579 (12): 2541–2545. PMID 15862287.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ Schriner SE, Linford NJ, Martin GM, Treuting P, Ogburn CE, Emond M, Coskun PE, Ladiges W, Wolf N, Van Remmen H, Wallace DC, Rabinovitch PS. (2005). "Extension of murine life span by overexpression of catalase targeted to mitochondria". SCIENCE. 308 (5730): 1909–1911. PMID 15879174.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Ku HH, Brunk UT, Sohal RS. (1993). "Relationship between mitochondrial superoxide and hydrogen peroxide production and longevity of mammalian species". FREE RADICAL BIOLOGY & MEDICINE. 15 (6): 621–627. PMID 8138188.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Barja G, Herrero A. (2000). "Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heart and brain of mammals". THE FASEB JOURNAL. 14 (2): 312–318. PMID 10657987.
  11. ^ Agarwal S, Sohal RS. (1996). "Relationship between susceptibility to protein oxidation, aging, and maximum life span potential of different species". EXPERIMENTAL GERONTOLOGY. 31 (3): 365–372. PMID 9415119.
  12. ^ Cortopassi GA, Wang E. (1996). "There is substantial agreement among interspecies estimates of DNA repair activity". MECHANISMS OF AGING AND DEVELOPMENT. 91 (3): 211–218. PMID 9055244.
  13. ^ Kurapati R, Passananti HB, Rose MR, Tower J. (2000). "Increased hsp22 RNA levels in Drosophila lines genetically selected for increased longevity". JOURNALS OF GERONTOLOGY SERIES A BIOLOGICAL SCIENCES AND MEDICAL SCIENCES. 55A (11): B552–B559. PMID 11078089.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ Friedman DB, Johnson TE. (1988). "A mutation in the age-1 gene in Caenorhabditis elegans lengthens life and reduces hermaphrodite fertility". GENETICS. 118 (1): 75–86. PMID 8608934.
  15. ^ Bluher M, Kahn BB, Kahn CR. (2003). "Extended longevity in mice lacking the insulin receptor in adipose tissue". SCIENCE. 299 (5606): 572–574. PMID 12543978.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Moore CJ, Schwartz AG. (1978). "Inverse correlation between species lifespan and capacity of cultured fibroblasts to convert benzo(a)pyrene to water-soluble metabolites". EXPERIMENTAL CELL RESEARCH. 116 (2): 359–364. PMID 101383.

See also

External links

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