Caenorhabditiselegans lifespan extension caused by treatment with an orally active ROS-generator is dependent on DAF-16 and SIR-2.1

• Published in: Biogerontology (Dordrecht) Vol. 11; no. 2; pp. 183 - 195
• Main Authors: Heidler, Tanja, Hartwig, Kai, Daniel, Hannelore, Wenzel, Uwe
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 2010
• Subjects: Biomedical and Life Sciences; Cell Biology; Developmental Biology; Geriatrics/Gerontology; Life Sciences; Research Article; Small heat-shock proteins; Reactive oxygen species; Hormesis; Stress response; Glutathione
• ISSN: 1389-5729; 1573-6768
• DOI: 10.1007/s10522-009-9239-x

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.