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Resources » Paper

Tanja Heidler et al. (2008) European Worm Meeting "A high glucose load in mev-1 Caenorhabditis elegans causes life span reduction by increased production of mitochondrial reactive oxygen species"

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  • Comments on Tanja Heidler et al. (2008) European Worm Meeting "A high glucose load in mev-1 Caenorhabditis elegans causes life span reduction by increased production of mitochondrial reactive oxygen species" (0)

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00033285

    Tanja Heidler, Hannelore Daniel, & Uwe Wenzel (2008). A high glucose load in mev-1 Caenorhabditis elegans causes life span reduction by increased production of mitochondrial reactive oxygen species presented in European Worm Meeting. Unpublished information; cite only with author permission.

    Reactive oxygen species (ROS) generated as by-products of mitochondrial. metabolism and respiration are considered to play a pivotal role in aging.. Otherwise mitochondrial ROS-formation has been suggested to cause hormetic. extension of life span by up-regulating distinct stress-response genes.. Using a liquid axenic medium we grow the ROS-sensitive Caenorhabditis. elegans mutant mev-1 in a high glucose medium and assessed the impact on. mitochondrial respiration and ROS-production and life span.. A high glucose load in mev-1 was associated with increased oxygen. consumption, enhanced mitochondrial ROS generation and a dramatic life span. reduction. The latter appeared to be caused by higher ROS levels since. scavenging of ROS by ascorbic acid blunted the effects of glucose on life. span reduction completely. The high glucose load obviously prevented. certain ROS-driven compensatory mechanisms to be activated. These feed-. forward stress response pathways mediated by nuclear DAF-16 translocation,. HSP-16.2 expression and increased glutathione synthesis, all were. suppressed in the presence of high glucose. Taken together, our results. suggest that increased glucose oxidation rates lead to enhanced. mitochondrial ROS-production with reduced life span and premature death in. mev-1. The high glucose load blunts via insulin/IGF-1 signalling a proper. activation of normal stress response mechanisms necessary to cope with. increased ROS production.


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