Maximum life span
Maximum life span is a measure of the maximum amount of time one or more members of a population has been observed to survive between birth and death. The term can also denote an estimate of the maximum amount of time that a member of a given species could survive between life and death, provided circumstances that are optimal to their longevity.
Most living species have at least one upper limit on the number of times cells can divide. This is called the Hayflick limit, although number of cell divisions does not strictly control lifespan (non-dividing cells and dividing cells lived over 122 years in the oldest known human).
In animal studies, maximum span is often taken to be the mean life span of the most long-lived 10% of a given cohort. By another definition, however, maximum life span corresponds to the age at which the oldest known member of a species or experimental group has died. Calculation of the maximum life span in the latter sense depends upon initial sample size.
Maximum life span contrasts with mean life span (average life span, life expectancy), and longevity. Mean life span varies with susceptibility to disease, accident, suicide and homicide, whereas maximum life span is determined by "rate of aging". Longevity refers only to the characteristics of the especially long lived members of a population, such as infirmities as they age or compression of morbidity, and not the specific life span of an individual.
The longest-living person whose dates of birth and death were verified to the modern norms of Guinness World Records and the Gerontology Research Group was Jeanne Calment, a French woman who lived to 122. The maximum (recorded) life span for humans has increased from 103 in 1798 to 110 years in 1898, 115 years in 1986, and 122.45 years since Calment's death in 1997 (See List of the verified oldest people and List of verified supercentenarians who died before 1980), among steady improvements in overall life expectancy. Reduction of infant mortality has accounted for most of this increased average longevity, but since the 1960s mortality rates among those over 80 years have decreased by about 1.5% per year. "The progress being made in lengthening lifespans and postponing senescence is entirely due to medical and public-health efforts, rising standards of living, better education, healthier nutrition and more salubrious lifestyles." Animal studies suggest that further lengthening of human lifespan could be achieved through "calorie restriction mimetic" drugs or by directly reducing food consumption. Although calorie restriction has not been proven to extend the maximum human life span, as of 2014, results in ongoing primate studies have demonstrated that the assumptions derived from rodents are valid in primates as well [Reference: Nature 01.04.2014].
No fixed theoretical limit to human longevity is apparent today. "A fundamental question in aging research is whether humans and other species possess an immutable life-span limit." "The assumption that the maximum human life span is fixed has been justified, [but] is invalid in a number of animal models and ... may become invalid for humans as well." Studies in the biodemography of human longevity indicate a late-life mortality deceleration law: that death rates level off at advanced ages to a late-life mortality plateau. That is, there is no fixed upper limit to human longevity, or fixed maximal human lifespan. This law was first quantified in 1939, when researchers found that the one-year probability of death at advanced age asymptotically approaches a limit of 44% for women and 54% for men.
It has also been observed that the VO2max value (a measure of the volume of oxygen flow to the cardiac muscle) decreases as a function of age. Therefore, the maximum lifespan of an individual can be determined by calculating when his or her VO2max value drops below the basal metabolic rate necessary to sustain life ---approximately 3 ml per kg per minute. Noakes (p. 84) notes that, on the basis of this hypothesis, athletes with a VO2max value between 50 and 60 at age 20 can be expected "to live for 100 to 125 years, provided they maintained their physical activity so that their rate of decline in VO2max remained constant.
In other animals
Small animals such as birds and squirrels rarely live to their maximum life span, usually dying of accidents, disease or predation. Grazing animals accumulate 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 or have effective defenses against predation, such as bird flight, tortoise shells, porcupine quills, or large primate brains.
The differences in life span between species demonstrate the role of genetics in determining maximum life span ("rate of aging"). The records (in years) are these:
- for common house mouse, 4
- for Norway rat, 7
- for dogs, 29 (See List of oldest dogs)
- for cats, 38
- for polar bears, 42 (Debby)
- for horses, 62
- for Asian elephants, 86
The longest-lived vertebrates have been variously described as
- Macaws (A parrot that can live up to 80–100 years in captivity)
- Koi (A Japanese species of fish, 200+ years, though generally not exceeding 250) Hanako was reportedly 226 years old upon her death.
- Greenland Sharks (A species of shark native to the North Atlantic, believed to be over 200 years)
- Tortoises (Galápagos tortoise) (190 years)
- Tuataras (a New Zealand reptile species, 100-200+ years)
- Eels, the so-called Brantevik eel (Swedish: Branteviksålen) is thought to have lived in a water well in southern Sweden since 1859, which makes it over 150 years old. It was reported that it had died in August 2014 at an age of 155
- Whales (Bowhead Whale) (Balaena mysticetus about 200 years)
- Although this idea was unproven for a time, recent research has indicated that bowhead whales recently killed still had harpoons in their bodies from about 1890, which, along with analysis of amino acids, has indicated a maximum life span, stated as "the 211 year-old bowhead could have been from 177 to 245 years old".
Invertebrate species which continue to grow as long as they live (e.g., certain clams, some coral species) can on occasion live hundreds of years:
- One species of jellyfish, Turritopsis dohrnii, reverts to a sexually immature stage after reproducing, rather than dying as in other jellyfish. Consequently the species is considered biologically immortal and has no maximum lifespan.
- There may be no natural limit to the Hydra's life span, but it is not yet clear how to estimate the age of a specimen.
- Flatworms, or Platyhelminthes, are known to be "almost immortal" as they have a great regeneration capacity, continuous growth and binary fission type cellular division.
- Lobsters are sometimes said to be biologically immortal because they don't seem to slow down, weaken, or lose fertility with age. However, due to the energy needed for moulting, they don't live indefinitely.
Plants are referred to as annuals which live only one year, biennials which live two years, and perennials which live longer than that. The longest-lived perennials, woody-stemmed plants such as trees and bushes, often live for hundreds and even thousands of years (one may question whether or not they may die of old age). A giant sequoia, General Sherman is alive and well in its third millennium. A Great Basin Bristlecone Pine called Methuselah is 4,845 years old (as of 2014) and the Bristlecone Pine called Prometheus was a little older still, at least 4,844 years (and possibly as old as 5,000 years), when it was cut down in 1964. The oldest known plant (possibly oldest living thing) is a clonal Quaking Aspen (Populus tremuloides) tree colony in the Fishlake National Forest in Utah called Pando at about 80,000 years.
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. "Maximum life span" here means the mean life span of the most long-lived 10% of a given cohort, 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 that contains all of the nutrients but only 40–60% of the calories that 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 caloric restriction is begun just before puberty. 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.
A few transgenic strains of mice have been created that have maximum life spans greater than that of wild-type or laboratory mice. The Ames and Snell mice, which have mutations in pituitary transcription factors and hence are deficient in Gh, LH, TSH, and secondarily IGF1, have extensions in maximal lifespan of up to 65%. To date, both in absolute and relative terms, these Ames and Snell mice have the maximum lifespan of any mouse not on caloric restriction (see below on GhR). Mutations/knockout of other genes affecting the GH/IGF1 axis, such as Lit, Ghr and Irs1 have also shown extension in lifespan, but much more modest both in relative and absolute terms. The longest lived laboratory mouse ever was a Ghr knockout mouse on caloric restriction, which lived to ~1800 days in the lab of Andrzej Bartke at Southern Illinois University. The maximum for normal B6 mice under ideal conditions is 1200 days.
Most biomedical gerontologists believe that biomedical molecular engineering will eventually extend maximum lifespan and even bring about rejuvenation.Anti-aging drugs are a potential tool for extending life.
Aubrey de Grey, a theoretical gerontologist, has proposed that aging can be reversed by Strategies for Engineered Negligible Senescence. De Grey has established The Methuselah Mouse Prize to award money to researchers who can extend the maximum life span of mice. Andrzej Bartke collected the prize for the GhR knockout mouse and Stephen Spindler collected the prize for extending the maximum lifespan of an adult mouse, using caloric restriction initiated late in life.
Correlation of DNA repair capacity with species maximum life span
||The neutrality of this article is disputed. (July 2014)|
Accumulated DNA damage appears to be a limiting factor in the determination of maximum life span. The theory that DNA damage is the primary cause of aging, and thus a principal determinant of maximum life span, has attracted increased interest in recent years. This is based, in part, on evidence in human and mouse that inherited deficiencies in DNA repair genes often cause accelerated aging. There is also substantial evidence that DNA damage accumulates with age in mammalian tissues, such as those of the brain, muscle, liver and kidney (reviewed by Bernstein et al. and see DNA damage theory of aging and DNA damage (naturally occurring)). One expectation of the theory (that DNA damage is the primary cause of aging) is that among species with differing maximum life spans, the capacity to repair DNA damage should correlate with lifespan. The first experimental test of this idea was by Hart and Setlow who measured the capacity of cells from seven different mammalian species to carry out DNA repair. They found that nucleotide excision repair capability increased systematically with species longevity. This correlation was striking and stimulated a series of 11 additional experiments in different laboratories over succeeding years on the relationship of nucleotide excision repair and life span in mammalian species (reviewed by Bernstein and Bernstein). In general, the findings of these studies indicated a good correlation between nucleotide excision repair capacity and life span. The association between nucleotide excision repair capability and longevity is strengthened by the evidence that defects in nucleotide excision repair proteins in humans and rodents cause features of premature aging, as reviewed by Diderich.
Further support for the theory that DNA damage is the primary cause of aging comes from study of Poly ADP ribose polymerases (PARPs). PARPs are enzymes that are activated by DNA strand breaks and play a role in DNA base excision repair. Burkle et al. reviewed evidence that PARPs, and especially PARP-1, are involved in maintaining mammalian longevity. The life span of 13 mammalian species correlated with poly(ADP ribosyl)ation capability measured in mononuclear cells. Furthermore, lymphoblastoid cell lines from peripheral blood lymphocytes of humans over age 100 had a significantly higher poly(ADP-ribosyl)ation capability than control cell lines from younger individuals.
Research data concerning maximum life span
- 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 free-radicals than rat mitochondria, despite the fact that both animals have similar metabolic rate and cardiac output
- For mammals there is a direct relationship between mitochondrial membrane fatty acid saturation and maximum life span
- Studies of the liver lipids of mammals and a bird (pigeon) show an inverse relationship between maximum life span and number of double bonds
- Selected species of birds and mammals show an inverse relationship between telomere rate of change (shortening) and maximum life span
- Maximum life span correlates negatively with antioxidant enzyme levels and free-radicals production and positively with rate of DNA repair
- Female mammals express more Mn−SOD and glutathione peroxidase antioxidant enzymes than males. This has been hypothesized as the reason they live longer However, mice entirely lacking in glutathione peroxidase 1 do not show a reduction in lifespan.
- The maximum life span of transgenic mice has been extended about 20% by overexpression of human catalase targeted to mitochondria
- 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
- 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
- A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span
- There is a direct correlation between DNA repair and maximum life span for mammalian species
- 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
- Overexpression of the enzyme which synthesizes glutathione in long-lived transgenic Drosophila (fruit-flies) extended maximum lifespan by nearly 50%
- A mutation in the age−1 gene of the nematode worm Caenorhabditis elegans increased mean life span 65% and maximum life span 110%. 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 °C and 65% extension at 27 °C.
- Fat-specific Insulin Receptor KnockOut (FIRKO) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18%.
- 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.
- 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.
- Aging brain
- American Aging Association
- Aubrey de Grey
- Biological immortality
- Calorie restriction
- Compression of morbidity
- DNA damage theory of aging
- Extreme longevity tracking
- Genetics of aging
- Hayflick limit
- Indefinite lifespan
- Life expectancy
- Life extension
- List of long-living organisms
- Methuselah Mouse Prize
- Michael Ristow
- Oldest people
- Strategies for Engineered Negligible Senescence (SENS)
- Gavrilov, Leonid A.; Gavrilova, Natalia S. (1991). The Biology of Life Span: A Quantitative Approach. New York: Harwood Academic. ISBN 978-3-7186-4983-9.[page needed]
- Brody, Jane E. (August 25, 2008). "Living Longer, in Good Health to the End". The New York Times. p. D7.[not in citation given]
- Vaupel, James W. (2010). "Biodemography of human ageing". Nature 464 (7288): 536–42. doi:10.1038/nature08984. PMID 20336136.
- Ingram, Donald K.; Roth, George S.; Lane, Mark A.; Ottinger, Mary Ann; Zou, Sige; Cabo, Rafael; Mattison, Julie A. (2006). "The potential for dietary restriction to increase longevity in humans: Extrapolation from monkey studies". Biogerontology 7 (3): 143–8. doi:10.1007/s10522-006-9013-2. PMID 16732404.
- Gavrilov, L. A.; Gavrilova, N. S. (1991). The Biology of Life Span: A Quantitative Approach. New York City: Starwood Academic Publishers. In Gavrilov, Leonid A.; Gavrilova, Natalia S.; Center on Aging, NORC/University of Chicago (June 2000). "Book Reviews: Validation of Exceptional Longevity" (PDF). Population Dev Rev 26 (2): 403–4. Retrieved 2009-05-18.
- Wilmoth, J. R.; Deegan, LJ; Lundström, H; Horiuchi, S (2000). "Increase of Maximum Life-Span in Sweden, 1861-1999". Science 289 (5488): 2366–8. doi:10.1126/science.289.5488.2366. PMID 11009426.
- Banks, D. A. (1997). "Telomeres, cancer, and aging. Altering the human life span". JAMA: the Journal of the American Medical Association 278 (16): 1345–8. doi:10.1001/jama.278.16.1345.
- Gavrilov, Leonid A.; Center on Aging, NORC/University of Chicago (2004-03-05). "Biodemography of Human Longevity (Keynote Lecture)". International Conference on Longevity. Retrieved 2009-05-18.
- Greenwood, M.; Irwin, J. O. (1939). "The biostatics of senility" (PDF). Human Biology 11: 1–23. Retrieved 2009-05-18.
- Noakes, T. (1985). The Lore of Running. Oxford University Press.
- B. M. Weon and J. H. Je (2009). "Theoretical estimation of maximum human lifespan". Biogerontology 10: 65–71. doi:10.1007/s10522-008-9156-4.
- "Longevity, Aging, and Life History of Mus musculus". Retrieved 2009-08-13.
- "World's oldest polar bear". Retrieved 2008-11-19.
- "Lin Wang, an Asian elephant (Elephas maximus) at Taipei Zoo". Retrieved 2009-08-13.
- "International Nishikigoi Promotion Center-Genealogy". Japan-nishikigoi.org. Retrieved 2009-04-11.
- Barton, Laura (2007-04-12). "The Guardian". London: The Guardian. Retrieved 2009-04-11.
- [dead link]
- Seed: Week In Science: 6/23 - 6/29[dead link]
- Tuatara#cite note-43
- "Brantevik Eels may be the world's oldest". 2008-04-11.
- "The world's oldest Eek dead - Lived 155 years in a well(Article in Swedish)". 2014-08-08.
- "125-Year-old New Bedford Bomb Fragment Found Embedded in Alaskan Bowhead Whale".
- "Bowhead Whales May Be the World's Oldest Mammals". 2001.
- "Bowhead Whales May Be the World's Oldest Mammals". 2007(reprint of 2001). Check date values in:
- John C. George, Jeffrey Bada, Judith Zeh, Laura Scott, Stephen E. Brown, Todd O'Hara, and Robert Suydam (1999). "Age and growth estimates of bowhead whales (Balaena mysticetus) via aspartic acid racemization". Can. J. Zool. 77 (4): 571–580. doi:10.1139/cjz-77-4-571.
- "Longest Living Animal? Clam -- 400 Years Old -- Found In Icelandic Waters".
- Philipp EE, Abele D (2010). "Masters of longevity: lessons from long-lived bivalves--a mini-review". Gerontology 56 (1): 55–65. doi:10.1159/000221004. PMID 19468199.
- Abele D, Strahl J, Brey T, Philipp EE (May 2008). "Imperceptible senescence: ageing in the ocean quahog Arctica islandica". Free Radic Res. 42 (5): 474–80. doi:10.1080/10715760802108849. PMID 18484411.
- Piraino, Stefano; F. Boero; B. Aeschbach; V. Schmid (1996). "Reversing the life cycle: medusae transforming into polyps and cell transdifferentiation in Turritopsis nutricula (Cnidaria, Hydrozoa)". Biological Bulletin (Biological Bulletin, vol. 190, no. 3) 190 (3): 302–312. doi:10.2307/1543022. JSTOR 1543022.
- Saló E. (2006). "The power of regeneration and the stem-cell kingdom: freshwater planarians (Platyhelminthes)". BioEssays 28 (5): 546–559. doi:10.1002/bies.20416. PMID 16615086.
- "Calorie Restriction in Humans - Calorie Restriction, Human Longevity and Life Expectancy". Longevity.about.com. 2007-12-06. Retrieved 2014-03-05.
- Koubova J, Guarente L. (2003). "How does calorie restriction work?". Genes & Development 17 (3): 313–321. doi:10.1101/gad.1052903. PMID 12569120.
- Mair W, Goymer P, Pletcher SD, Partridge L. (2003). "Demography of dietary restriction and death in Drosophila". Science 301 (5640): 1731–1733. doi:10.1126/science.1086016. PMID 14500985.
- Kaeberlein, Matt (2010). "Resveratrol and rapamycin:are they anti-aging drugs?". BioEssays 32 (2): 96–99. doi:10.1002/bies.200900171. PMID 20091754.
- Hoeijmakers, JH (2009). "DNA damage, aging, and cancer". N Engl J Med 361 (15): 1475–1485. doi:10.1056/NEJMra0804615. PMID 19812404.
- Diderich K, Alanazi M, Hoeijmakers JH (2011). Premature aging and cancer in nucleotide excision repair-disorders. DNA Repair (Amst) 10(7):772-780. doi: 10.1016/j.dnarep.2011.04.025. Review. PMID 21680258
- Freitas AA, de Magalhães JP (2011). A review and appraisal of the DNA damage theory of ageing. Mutat Res 728(1-2):12-22. Review. doi:10.1016/j.mrrev.2011.05.001 PMID 21600302
- Bernstein H, Payne CM, Bernstein C, Garewal H, Dvorak K (2008). Cancer and aging as consequences of un-repaired DNA damage. In: New Research on DNA Damages (Editors: Honoka Kimura and Aoi Suzuki) Nova Science Publishers, Inc., New York, Chapter 1, pp. 1-47. ISBN 1604565810 ISBN 978-1604565812
- Hart, RW; Setlow, RB (1974). "Correlation between deoxyribonucleic acid excision-repair and life-span in a number of mammalian species". Proc Natl Acad Sci U S A 71 (6): 2169–2173. doi:10.1073/pnas.71.6.2169. PMID 4526202.
- Bernstein C, Bernstein H. (1991) Aging, Sex, and DNA Repair. Academic Press, San Diego. ISBN 0120928604 ISBN 978-0120928606
- Bürkle A, Brabeck C, Diefenbach J, Beneke S (2005). The emerging role of poly(ADP-ribose) polymerase-1 in longevity. Int J Biochem Cell Biol 37(5):1043-1053. Review. doi:10.1016/j.biocel.2004.10.006 PMID 15743677
- 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. doi:10.1016/S0047-6374(97)00076-6. PMID 9379714.
- Pamplona R, Portero-Otin M, Riba D, Ruiz C, Prat J, Bellmunt MJ, Barja G. (1 October 1998). "Mitochondrial membrane peroxidizability index is inversely related to maximum life span in mammals". Journal of Lipid Research 39 (2): 1989–1994. PMID 9788245.
- 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.
- Haussmann MF, Winkler DW, O'Reilly KM, Huntington CE, Nisbet IC, Vleck CM (2003). "Telomeres shorten more slowly in long-lived birds and mammals than in short-lived ones". Proceedings. Biological Sciences / the Royal Society 270 (1522): 1387–1392. doi:10.1098/rspb.2003.2385. PMC 1691385. PMID 12965030.
- 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. doi:10.1007/s003600050131. PMID 9591361.
- 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. doi:10.1016/j.febslet.2005.03.090. PMID 15862287.
- 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. doi:10.1126/science.1106653. PMID 15879174.
- 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. doi:10.1016/0891-5849(93)90165-Q. PMID 8138188.
- Barja G, Herrero A. (1 February 2000). "Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heart and brain of mammals". FASEB J. 14 (2): 312–318. PMID 10657987.
- 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. doi:10.1016/0531-5565(95)02039-X. PMID 9415119.
- 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. doi:10.1016/S0047-6374(96)01788-5. PMID 9055244.
- 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.
- Orr WC, Radyuk SN, Prabhudesai L, Toroser D, Benes JJ, Luchak JM, Mockett RJ, Rebrin I, Hubbard JG, Sohal RS (2005). "Overexpression of glutamate-cysteine ligase extends life span in Drosophila melanogaster". The Journal of Biological Chemistry 280 (45): 37331–37338. doi:10.1074/jbc.M508272200. PMID 16148000.
- Friedman DB, Johnson TE. (1 January 1988). "A mutation in the age-1 gene in Caenorhabditis elegans lengthens life and reduces hermaphrodite fertility". Genetics 118 (1): 75–86. PMC 1203268. PMID 8608934.
- Bluher M, Kahn BB, Kahn CR. (2003). "Extended longevity in mice lacking the insulin receptor in adipose tissue". SCIENCE 299 (5606): 572–574. doi:10.1126/science.1078223. PMID 12543978.
- 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. doi:10.1016/0014-4827(78)90459-7. PMID 101383.
- "Publication demonstrating that oxidative stress is promoting life span". Cellmetabolism.org. Retrieved 2010-11-04.
- AnAge Database
- Informational website on the biology of aging.
- Mechanisms of Aging
- The animals with the longest and shortest life spans