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Heidler, T, Hartwig, K, Daniel, H and Wenzel, U (2010) Caenorhabditis elegans lifespan extension caused by treatment with an orally active ROS-generator is dependent on DAF-16 and SIR-2.1. Biogerontology 11:183-95


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.


PubMed Online version:10.1007/s10522-009-9239-x


Animals; Caenorhabditis elegans/physiology; Caenorhabditis elegans Proteins/genetics; Caenorhabditis elegans Proteins/metabolism; Dose-Response Relationship, Drug; Enzyme Inhibitors/pharmacology; Gene Deletion; Heat-Shock Proteins/metabolism; Kaplan-Meier Estimate; Longevity/drug effects; Models, Animal; Naphthoquinones/pharmacology; Oxidative Stress/physiology; RNA Interference; Reactive Oxygen Species/metabolism; Sirtuins/genetics; Sirtuins/metabolism; Transcription Factors/genetics; Transcription Factors/metabolism



Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

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