Open AccessCalorie restriction delays lipid oxidative damage in Drosophila melanogaster
Author(s) -
Zheng Jianyu,
Mutcherson Raye,
Helfand Stephen L.
Publication year - 2005
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/j.1474-9726.2005.00159.x
Subject(s) - calorie restriction , oxidative stress , drosophila melanogaster , biology , lipid peroxidation , oxidative phosphorylation , oxidative damage , ageing , dna damage , drosophila (subgenus) , lipid oxidation , biochemistry , microbiology and biotechnology , antioxidant , genetics , endocrinology , gene , dna
Summary The oxidative stress hypothesis predicts that the accumulation of oxidative damage to a variety of macromolecules is the molecular trigger driving the process of aging. Although an inverse relationship between oxidative damage and lifespan has been established in several different species, the precise relationship between oxidative damage and aging is not fully understood. Drosophila melanogaster is a favored model organism for aging research. Environmental interventions such as ambient temperature and calorie restriction can alter adult lifespan to provide an excellent system to examine the relationship between oxidative damage, aging and lifespan. We have developed an enzyme‐linked immunosorbent assay (ELISA) using commercially available reagents for measuring 4‐hydroxy‐2‐nonenal (HNE) in proteins, a marker for oxidative damage to lipids, and present data in flies to show that HNE adducts accumulate in an age‐dependent manner. With immunohistology, we also find the primary site of HNE accumulation is the pericerebral fat body, where induction of dFOXO was recently shown to retard aging. When subjected to environmental interventions that shorten lifespan, such as elevated ambient temperature, the chronological accumulation of HNE adduct is accelerated. Conversely, interventions that extend lifespan, such as lower ambient temperature or low calorie diets, slow the accumulation of HNE adduct. These studies associate damage from lipid peroxidation with aging and lifespan in Drosophila and show that calorie restriction in flies, as in mammals, slows the accumulation of lipid related oxidative damage.