DiscussionLifespan is not determined by metabolic rate: evidence from fishes and C. elegans
Section snippets
Acknowledgments
These studies were supported by the National Institutes on Aging.
References (18)
- et al.
The effect of dietary restriction of varying duration on survival, tumor patterns, immune function, and body temperature in B10C3F1 female mice
J. Gerontol.
(1983) - et al.
Rates of behavior and aging specified by mitochondrial function during development
Science
(2002) - et al.
Effects of food restriction on aging: separation of food intake and adiposity
Proc. Natl Acad. Sci. USA
(1984) - et al.
Gene expression profile of aging and its retardation by caloric restriction
Science
(1999) - et al.
Transcriptional profiles associated with aging and middle age-onset caloric restriction in mouse hearts
Proc. Natl Acad. Sci. USA
(2002) - et al.
Increased growth and life-span with lowered ambient temperature in the annual fish, Cynolebia adloffi
Nature
(1966) - et al.
Observations on the lifespans of several species of annual fishes and of the world's smallest fishes
Exp. Gerontol.
(1970) - et al.
The effect of lowered body temperature on lifespan and immune and non-immune processes
Gerontologia
(1972) - et al.
Mid-life temperature-transfer effects on life-span of annual fish
J. Gerontol.
(1975)
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SOD isoforms play no role in lifespan in ad lib or dietary restricted conditions, but mutational inactivation of SOD-1 reduces life extension by cold
2009, Mechanisms of Ageing and DevelopmentLowered methionine ingestion as responsible for the decrease in rodent mitochondrial oxidative stress in protein and dietary restriction. Possible implications for humans
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