<Emphasis Type="Italic">Caenorhabditis</Emphasis><Emphasis Type="Italic">elegans</Emphasis> lifespan extension caused by treatment with an orally active ROS-generator is dependent on DAF-16 and SIR-2.1 |
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Authors: | Tanja Heidler Kai Hartwig Hannelore Daniel Uwe Wenzel |
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Institution: | (1) Department of Food and Nutrition, Molecular Nutrition Unit, Technical University of Munich, Am Forum 5, 85350 Freising, Germany;(2) Molecular Nutrition Research, Interdisciplinary Research Center, Justus-Liebig-University of Giessen, Heinrich-Buff-Ring 26-32, 35392 Giessen, Germany; |
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Abstract: | In Caenorhabditis
elegans pretreatment with juglone, a generator of reactive oxygen species (ROS) provides a subsequently increased ROS-resistance.
We investigated whether juglone at low or high concentrations when provided via the oral route in a liquid axenic medium affects
normal lifespan of C.
elegans. High juglone concentrations led to premature death, low concentrations were tolerated well and caused a prolongation of
lifespan. Lifespan extension under moderate oxidative stress was associated with increased expression of small heat-shock
protein HSP-16.2, enhanced glutathione levels, and nuclear translocation of DAF-16. Silencing or deletion of DAF-16 prevented
the juglone-induced adaptations. RNA-interference for SIR-2.1 had the same effects as the deletion of DAF-16 but did not affect
nuclear accumulation of DAF-16. Our studies demonstrate that DAF-16- and SIR-2.1-dependent alterations in gene expression
after a ROS challenge lead to a lifespan extension in C.
elegans as long as the stressor concentration does not exceed the saturable protective capacity. |
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