p66shc inactivation modifies rns production, regulates sirt3 activity, and improves mitochondrial homeostasis, delaying the aging process in mouse brain
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ID: 234785
2018
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Abstract
Programmed and damage aging theories have traditionally been conceived as stand-alone schools of thought. However, the p66Shc adaptor protein has demonstrated that aging-regulating genes and reactive oxygen species (ROS) are closely interconnected, since its absence modifies metabolic homeostasis by providing oxidative stress resistance and promoting longevity. p66Shc(−/−) mice are a unique opportunity to further comprehend the bidirectional relationship between redox homeostasis and the imbalance of mitochondrial biogenesis and dynamics during aging. This study shows that brain mitochondria of p66Shc(−/−) aged mice exhibit a reduced alteration of redox balance with a decrease in both ROS generation and its detoxification activity. We also demonstrate a strong link between reactive nitrogen species (RNS) and mitochondrial function, morphology, and biogenesis, where low levels of ONOO− formation present in aged p66Shc(−/−) mouse brain prevent protein nitration, delaying the loss of biological functions characteristic of the aging process. Sirt3 modulates age-associated mitochondrial biology and function via lysine deacetylation of target proteins, and we show that its regulation depends on its nitration status and is benefited by the improved NAD+/NADH ratio in aged p66Shc(−/−) brain mitochondria. Low levels of protein nitration and acetylation could cause the metabolic homeostasis maintenance observed during aging in this group, thus increasing its lifespan.
| Reference Key |
prez2018oxidativep66shc
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| Authors | ;Hernán Pérez;Paola Vanesa Finocchietto;Yael Alippe;Inés Rebagliati;María Eugenia Elguero;Nerina Villalba;Juan José Poderoso;María Cecilia Carreras |
| Journal | journal of aoac international |
| Year | 2018 |
| DOI |
10.1155/2018/8561892
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