Abstract
OBJECTIVE:The free radical theory of aging suggests that cellular oxidative damage caused by free radicals is a leading cause of aging. In the present study, we examined the effects of a well-known anti-oxidant amino acid derivative, selenocysteine, in response to environmental stress and aging using Caenorhabditis elegans as a model system.METHOD:The response to oxidative stress induced by H2O2 or ultraviolet irradiation was compared between the untreated control and selenocysteine-treated groups. The effect of selenocysteine on lifespan and fertility was then determined. To examine the effect of selenocysteine on muscle aging, we monitored the change in motility with aging in both the untreated control and selenocysteine-treated groups.RESULTS:Dietary supplementation with selenocysteine significantly increased resistance to oxidative stress. Survival after ultraviolet irradiation was also increased by supplementation with selenocysteine. Treatment with selenocysteine confers a longevity phenotype without an accompanying reduction in fertility, which is frequently observed in lifespan-extending interventions as a trade-off in C. elegans. In addition, the age-related decline in motility was significantly delayed by supplementation of selenocysteine.CONCLUSION:These findings suggest that dietary supplementation of selenocysteine can modulate response to stressors and lead to lifespan extension, thus supporting the free radical theory of aging.
Highlights
Aging is one of the most complex biological pathways, with hundreds of theories attempting to explain the aging process
6.7±3.33% of worms survived in the untreated control groups, whereas 28.9±9.09 (p=0.083) and 44.4±5.88% (p=0.005) of worms survived in the experimental groups pre-treated with 2.5 and 5 mM selenocysteine, respectively (Figure 1)
Mutations in daf-2, a receptor for insulin/IGF-1-like ligand, and age-1, an intracellular adaptor molecule involved in insulin/IGF-1-like signaling, lead to an extended lifespan in C. elegans [27]
Summary
Aging is one of the most complex biological pathways, with hundreds of theories attempting to explain the aging process. The mitochondrial decline theory of aging emphasizes the function of the mitochondria in aging. Other well-known theories of aging include the genomic instability theory, Hayflick limit theory, telomerase theory, and membrane theory [3, 4]. Despite these various theories, there is no single theory of aging that can explain all phenomena observed in the aging process. People believe that the various theories of aging are closely inter-related [4]
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