Research Article

Biogerontology

, Volume 11, Issue 2, pp 183-195

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

  • Tanja HeidlerAffiliated withDepartment of Food and Nutrition, Molecular Nutrition Unit, Technical University of Munich
  • , Kai HartwigAffiliated withDepartment of Food and Nutrition, Molecular Nutrition Unit, Technical University of Munich
  • , Hannelore DanielAffiliated withDepartment of Food and Nutrition, Molecular Nutrition Unit, Technical University of Munich
  • , Uwe WenzelAffiliated withMolecular Nutrition Research, Interdisciplinary Research Center, Justus-Liebig-University of Giessen Email author 

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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.

Keywords

Caenorhabditis elegans Hormesis Reactive oxygen species Stress response Small heat-shock proteins Glutathione