Abstract
Human longevity is a polygenic and multifactorial trait. Pathways related to lifespan are complex and involve molecular, cellular, and environmental processes. In this analytical observational study, we evaluated the relationship between environment factors, oxidative stress status, DNA integrity level, and the association of FOXO3 (rs2802292), SOD2 (rs4880), APOE (rs429358 and rs7412), and SIRT1 (rs2273773) polymorphisms with longevity in oldest-old individuals from southeastern Brazil. We found an association between the FOXO3 GG genotype and gender. While lifestyle, anthropometric, and biochemical characteristics showed significant results, DNA damage and oxidative stress were not related to lifespan. We found that long-lived individuals with FOXO3 GT genotype had low levels of triglycerides. This study is the first to demonstrate that FOXO3 could be a candidate gene for longevity in the Brazilian population. These results are important in terms of provisions of health care for age-related diseases and lifespan, and provide insight for further research on epigenetic, gene regulation, and expression in oldest-old individuals.
Highlights
Life expectancy in the world has more than doubled in the last two centuries
The chosen age range of controls is in accordance with studies, which claim that elderly people with age close to the lifespan of a certain population are more prone to genetic factors to environmental factors (Willcox et al, 2008; Anselmi et al, 2009; Flachsbart et al, 2009)
The present study aimed to evaluate the association of Forkhead box O3 (FOXO3), SOD2, APOE, and SIRT1 polymorphisms with longevity and the relationship between genomic damage and oxidative stress status in elderly people of southeastern Brazil
Summary
Life expectancy in the world has more than doubled in the last two centuries. People aged 85 years or more, often designated the “oldest-old”, are the fastest-growing age group. Longevity is a multifactorial condition, affected by environmental and genetic factors, as well as by oxidative and genomic damage. Several hypotheses have been postulated to explain aging and lifespan, which have attracted widespread scientific and public interest (Brooks-Wilson, 2013; Simm and Klotz, 2015). The reactive oxygen species (ROS) theory of aging is related to oxidative stress and macromolecule damage.
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