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Maximum life span

Maximum life span (or, for humans, maximum reported age at death) is a measure of the maximum amount of time one or more members of a population have 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 birth and death, provided circumstances that are optimal to that member's longevity.

Most living species have an upper limit on the number of times somatic cells not expressing telomerase can divide. This is called the Hayflick limit, although this number of cell divisions does not strictly control lifespan.

Definition[edit]

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 the initial sample size.[1]


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".[2][3] 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.

for , 4[26]

common house mouse

for , 3.8[27]

Brown rat

for , 29 (See List of oldest dogs)[28]

dogs

for , 38 (See List of oldest cats)[29]

cats

for , 43[30]

common cranes

for , 42[31] (Debby)

polar bears

for , 62[32]

horses

for , 86[33]

Asian elephants

A comparison of the heart 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[66]

mitochondria

For there is a direct relationship between mitochondrial membrane fatty acid saturation and maximum life span[67]

mammals

Studies of the lipids of mammals and a bird (pigeon) show an inverse relationship between maximum life span and number of double bonds[68]

liver

Selected species of birds and mammals show an inverse relationship between rate of change (shortening) and maximum life span[69]

telomere

Maximum life span correlates negatively with enzyme levels and free-radicals production and positively with rate of DNA repair[70]

antioxidant

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.

[71]

The maximum life span of mice has been extended about 20% by overexpression of human catalase targeted to mitochondria[72]

transgenic

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

[73]

A study of 8 non-primate mammals showed an inverse correlation between maximum life span and oxidative damage to mtDNA () in heart & brain[74]

mitochondrial DNA

A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span

[75]

There is a direct correlation between DNA repair and maximum life span for species[76]

mammalian

(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[77]

Drosophila

Overexpression of the enzyme which synthesizes in long-lived transgenic Drosophila (fruit-flies) extended maximum lifespan by nearly 50%[78]

glutathione

A mutation in the age−1 gene of the worm Caenorhabditis elegans increased mean life span 65% and maximum life span 110%.[79] 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.

nematode

Fat-specific Insulin Receptor (FIRKO) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18%.[80]

KnockOut

The capacity of mammalian species to detoxify the chemical benzo(a)pyrene to a water-soluble form also correlates well with maximum life span.[81]

carcinogenic

Short-term induction of 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.[82]

oxidative stress

Extreme longevity tracking

Genetics of aging

Longevity quotient

(SENS)

Strategies for engineered negligible senescence

Anage Database

Informational website on the biology of aging

Mechanisms of Aging