You can’t beat the clock : oxidative stress and period mutants in Drosophila melanogaster Public Deposited


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  • The free-radical theory of aging proposes that intracellular accumulation of oxidative damage caused by reactive oxygen species (ROS) is responsible for the process of senescence. ROS are produced during normal aerobic metabolism and have been shown to cause numerous cellular and sub-cellular defects that lead to termination of the cell cycle and, in extreme cases, to apoptosis (cell death). Previous research has suggested that important antioxidant enzymes and other low molecular weight antioxidants may exhibit differential levels of expression throughout the day/night cycle. These expression trends appear to be under the control of biological clock genes, which interact to generate circadian rhythms within organisms. There are several clock genes that are essential for proper clock function in Drosophila melanogaster, the most important of which are period (per) and timeless (tim); a null mutation in either of these genes causes a loss of clock function in the organism. Since biological rhythms regulate many important processes, they may be involved in the antioxidant defense system. The overarching hypothesis of this study was that the loss of biological rhythmicity exhibited by mutant flies may render them more susceptible to the negative effects associated with ROS exposure. The main objective of the current study was to investigate the intersection of circadian rhythmicity, oxidative stress, and the process of aging in Drosophila. We show that period mutants have increased susceptibility to oxidative stress, when compared to their wildtype (CSP) counterparts, indicating that the period gene is somehow involved in the oxidative stress response system. However, experiments on the enzyme catalase show that one rhythmically expressed enzyme cannot explain the physiological response exhibited by the organism. Accumulation of oxidative damage, as measured by protein carbonylation, appears to be rhythmic, suggesting a possible explanation for the differential susceptibility to exogenous oxidative stress.
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  • description.provenance : Made available in DSpace on 2007-11-01T19:48:17Z (GMT). No. of bitstreams: 1 Thesis Complete davis.PDF: 2203286 bytes, checksum: cf3758432dd3654e5aa62422bb4bd647 (MD5)
  • description.provenance : Submitted by Heather Boren (borenh) on 2007-11-01T18:14:52Z No. of bitstreams: 1 Thesis Complete davis.PDF: 2203286 bytes, checksum: cf3758432dd3654e5aa62422bb4bd647 (MD5)


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