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• W2080346572 startingPage "156" @default.
• W2080346572 abstract "Since the initial identification of reactive oxygen species (ROS) as the major factor in aging, many studies have provided evidence for the central role of mitochondria in longevity. A few years ago, an unexpected finding showed that the inactivation of the mitochondrial respiratory chain (MRC) in Caenorhabditis elegans, during the developmental stages only, extended lifespan. Activation of this mitochondrial pathway affecting aging (MIT) is associated with several phenotypic features: increased longevity, increased time of development, decreased fertility/fecundity and reduced adult size. Here, we investigated this pathway in another model organism, Drosophila melanogaster. To assess the role of mitochondrial activity in the Drosophila aging process, we partially inactivated the MRC using RNA interference (RNAi) during larval stages. Developmental perturbation of the respiratory process prolonged development, increased lethality during developmental stage, reduced both fecundity and fertility and slightly reduced individual weight. However, in contrast to the nematode, this genetic intervention either shortened or had no effect on lifespan, depending on the level of gene inactivation. Thus, the effects of MRC disruption during development on aging differ between species. We discuss the possible origins of such differences." @default.
• W2080346572 created "2016-06-24" @default.
• W2080346572 creator A5046580490 @default.
• W2080346572 creator A5062742665 @default.
• W2080346572 creator A5067562053 @default.
• W2080346572 date "2010-02-01" @default.
• W2080346572 modified "2023-10-18" @default.
• W2080346572 title "Mitochondrial electron transport chain dysfunction during development does not extend lifespan in Drosophila melanogaster" @default.
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• W2080346572 doi "https://doi.org/10.1016/j.mad.2010.01.004" @default.
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