Nanami Senoo-Matsuda

TL;DR: The results indicate that mev-1 governs the rate of ageing by modulating the cellular response to oxidative stress, which may cause an indirect increase in superoxide levels, which in turn leads to oxygen hypersensitivity and premature ageing.

TL;DR: Important biochemical changes in mev-1 animals are reported that serve to explain their abnormalities under normoxic conditions: an overproduction of superoxide anion from mitochondria; and a reciprocal reduction in glutathione content even under atmospheric oxygen.

TL;DR: Data suggest that exogenously supplied CoQ(10) can play a significant anti-aging function and may do so either by acting as an antioxidant to dismutate the free radical superoxide anion or by reducing the uncoupling of reactions during election transport that could otherwise result in superoxideAnion production.

TL;DR: It is shown that mev-1 mutants are defective in succinate-coenzyme Q oxidoreductase, possess ultrastructural mitochondrial abnormalities (especially in muscle cells), show a loss of membrane potential, have altered CED-9 and Cyt-1 protein levels under hyperoxia, and contain ced-3-and-ced-4-dependent supernumerary apoptotic cells.

TL;DR: It is shown that both mev-1 and gas-1 mutants overproduce superoxide anion in isolated sub-mitochondrial particles, which probably explains their hypersensitivity to oxidative stress.