Editing Maximum life span (section)

==Research data==
* A comparison of the heart [[mitochondria]] in rats (7-year maximum life span) and pigeons (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 | vauthors = 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 Ageing and Development | volume = 98 | issue = 2 | pages = 95–111 | date = November 1997 | pmid = 9379714 | doi = 10.1016/S0047-6374(97)00076-6 | s2cid = 20424838 }}</ref>
* For [[mammal]]s there is a direct relationship between [[mitochondrial membrane]] [[fatty acid]] saturation and maximum life span<ref>{{cite journal |vauthors=Pamplona R, Portero-Otín M, Riba D, Ruiz C, Prat J, Bellmunt MJ, Barja G |date=October 1998 |title=Mitochondrial membrane peroxidizability index is inversely related to maximum life span in mammals |journal=[[Journal of Lipid Research]] |volume=39 |issue=10 |pages=1989–94 |doi=10.1016/S0022-2275(20)32497-4 |pmid=9788245 |doi-access=free}}</ref>
* 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 | vauthors = Pamplona R, Portero-Otín M, Riba D, Requena JR, Thorpe SR, López-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 = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 55 | issue = 6 | pages = B286–91 | date = June 2000 | pmid = 10843345 | doi=10.1093/gerona/55.6.b286| doi-access = free }}</ref>
* Selected species of birds and mammals show an inverse relationship between [[telomere]] rate of change (shortening) and maximum life span<ref>{{cite journal | vauthors = Haussmann MF, Winkler DW, O'Reilly KM, Huntington CE, Nisbet IC, Vleck CM | title = Telomeres shorten more slowly in long-lived birds and mammals than in short-lived ones | journal = Proceedings. Biological Sciences | volume = 270 | issue = 1522 | pages = 1387–92 | date = July 2003 | pmid = 12965030 | pmc = 1691385 | doi = 10.1098/rspb.2003.2385 }}</ref>
* Maximum life span correlates negatively with [[antioxidant]] [[enzyme]] levels and [[radical (chemistry)|free-radicals]] production and positively with rate of [[DNA repair]]<ref>{{cite journal | vauthors = Perez-Campo R, López-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 | pages = 149–58 | date = April 1998 | pmid = 9591361 | doi = 10.1007/s003600050131 | s2cid = 12080649 }}</ref>
* Female mammals express more [[Mn−SOD]] and [[glutathione peroxidase]] antioxidant enzymes than males. This has been hypothesized as the reason they live longer.<ref>{{cite journal | vauthors = Viña J, Borrás C, Gambini J, Sastre J, Pallardó 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 | pages = 2541–5 | date = May 2005 | pmid = 15862287 | doi = 10.1016/j.febslet.2005.03.090 | doi-access = free }}</ref> However, mice entirely lacking in [[GPX1|glutathione peroxidase&nbsp;1]] do not show a reduction in lifespan.
* The maximum life span of [[Genetically modified organism|transgenic]] mice has been extended about 20% by overexpression of human [[catalase]] targeted to mitochondria<ref>{{cite journal | vauthors = 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 | volume = 308 | issue = 5730 | pages = 1909–11 | date = June 2005 | pmid = 15879174 | doi = 10.1126/science.1106653 | bibcode = 2005Sci...308.1909S | s2cid = 38568666 }}</ref>
* 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<ref>{{cite journal | vauthors = Ku HH, Brunk UT, Sohal RS | title = Relationship between mitochondrial superoxide and hydrogen peroxide production and longevity of mammalian species | journal = Free Radical Biology & Medicine | volume = 15 | issue = 6 | pages = 621–7 | date = December 1993 | pmid = 8138188 | doi = 10.1016/0891-5849(93)90165-Q }}</ref>
* A study of 8 non-primate mammals showed an inverse correlation between maximum life span and [[oxidative damage]] to mtDNA ([[mitochondrial DNA]]) in heart & brain<ref>{{cite journal | vauthors = 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 = FASEB Journal | volume = 14 | issue = 2 | pages = 312–8 | date = February 2000 | pmid = 10657987 | url = http://www.fasebj.org/cgi/content/full/14/2/312 | doi=10.1096/fasebj.14.2.312| doi-access = free | s2cid = 14826037 }}</ref>
* 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 | vauthors = 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 | pages = 365–72 | year = 1996 | pmid = 9415119 | doi = 10.1016/0531-5565(95)02039-X | s2cid = 21564827 }}</ref>
* There is a direct correlation between DNA repair and maximum life span for [[mammal]]ian species<ref>{{cite journal | vauthors = Cortopassi GA, Wang E | title = There is substantial agreement among interspecies estimates of DNA repair activity | journal = Mechanisms of Ageing and Development | volume = 91 | issue = 3 | pages = 211–8 | date = November 1996 | pmid = 9055244 | doi = 10.1016/S0047-6374(96)01788-5 | s2cid = 24364141 }}</ref>
* [[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% greater than that of controls<ref>{{cite journal | vauthors = Kurapati R, Passananti HB, Rose MR, Tower J | title = Increased hsp22 RNA levels in Drosophila lines genetically selected for increased longevity | journal = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 55 | issue = 11 | pages = B552–9 | date = November 2000 | pmid = 11078089 | doi=10.1093/gerona/55.11.b552| doi-access = free }}</ref>
* Overexpression of the enzyme which synthesizes [[glutathione]] in long-lived [[Genetically modified organism|transgenic]] ''Drosophila'' (fruit-flies) extended maximum lifespan by nearly 50%<ref>{{cite journal | vauthors = Orr WC, Radyuk SN, Prabhudesai L, Toroser D, Benes JJ, Luchak JM, Mockett RJ, Rebrin I, Hubbard JG, Sohal RS | title = Overexpression of glutamate-cysteine ligase extends life span in Drosophila melanogaster | journal = The Journal of Biological Chemistry | volume = 280 | issue = 45 | pages = 37331–8 | date = November 2005 | pmid = 16148000 | doi = 10.1074/jbc.M508272200 | doi-access = free }}</ref>
* A mutation in the '''age−1''' gene of the [[nematode]] worm ''[[Caenorhabditis elegans]]'' increased [[mean life span]] 65% and maximum life span 110%.<ref>{{cite journal | vauthors = 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 | pages = 75–86 | date = January 1988 | doi = 10.1093/genetics/118.1.75 | pmid = 8608934 | pmc = 1203268 | url = http://www.genetics.org/cgi/reprint/118/1/75 }}</ref> However, the degree of lifespan extension in relative terms by both the age-1 and daf-2 mutations is strongly dependent on ambient temperature, with ≈10% extension at 16&nbsp;°C and 65% extension at 27&nbsp;°C.
* Fat-specific Insulin Receptor [[Knockout mouse|KnockOut]] (FIRKO) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18%.<ref>{{cite journal | vauthors = Blüher M, Kahn BB, Kahn CR | title = Extended longevity in mice lacking the insulin receptor in adipose tissue | journal = Science | volume = 299 | issue = 5606 | pages = 572–4 | date = January 2003 | pmid = 12543978 | doi = 10.1126/science.1078223 | bibcode = 2003Sci...299..572B | s2cid = 24114184 }}</ref>
* The capacity of mammalian species to detoxify the [[carcinogenic]] chemical [[Benzo(a)pyrene|benzo[a]pyrene]] to a water-soluble form also correlates well with maximum life span.<ref>{{cite journal | vauthors = 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 | pages = 359–64 | date = October 1978 | pmid = 101383 | doi = 10.1016/0014-4827(78)90459-7 }}</ref>
* Short-term induction of [[oxidative stress]] due to [[calorie restriction]] increases life span in ''Caenorhabditis elegans'' by promoting stress defense, specifically by inducing an enzyme called catalase. As shown by [[Michael Ristow]] and co-workers nutritive antioxidants completely abolish this extension of life span by inhibiting a process called [[mitohormesis]].<ref>{{cite journal |vauthors=Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M |date=October 2007 |title=Glucose Restriction Extends ''Caenorhabditis elegans'' Life Span by Inducing Mitochondrial Respiration and Increasing Oxidative Stress |journal=Cell Metabolism |volume=6 |issue=4 |pages=280–293 |doi=10.1016/j.cmet.2007.08.011 |pmid=17908557 |doi-access=free}}</ref>