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O P E N A C C E S S S O U R C E (.PDF) : bioRxiv
Abstract
Resveratrol consumption has linked with normalization of the risk factors of some diseases such as colon cancer and type 2 diabetes. The antioxidant phenotype caused by resveratrol has recognized as a key piece in the health benefits exerted by this phytochemical. Although the antioxidant activity showed by resveratrol has attributed at the molecule per se, recent evidence indicates that the antioxidant effect occasioned by resveratrol could be associated with a pro-oxidant mechanism.
The hypothesis that resveratrol inhibits complex III of the electron transport chain as its main target suggests that resveratrol increases reactive oxygen species (ROS) generation produces via reverse electron transport. This idea also explains that cells respond to the oxidative damage caused by resveratrol, inducing their antioxidant systems. The free radical theory of aging postulates that organisms age due to the accumulation of the harmful effects of ROS in cells.
For these reasons, we hypothesize that resveratrol shortens the chronological life span (CLS) of Saccharomyces cerevisiae due to a pro-oxidant activity. Herein, we provide evidence that 100 μM resveratrol supplementation at 5% glucose: 1) shorted the CLS of CTT1 and YAP1 genes deleted strains; 2) decreased the H2O2 release in the WT strain, and maintain unaltered the H2O2 release in the ctt1∆ strain; 3) lessened exponential growth of ctt1∆ strain, which was reverted with the adding of GSH; 4) increased catalase activity in the WT strain, a phenotype that was not observed in the ctt1∆ strain. Altogether, these results indicate that resveratrol decreases CLS by a pro-oxidant mechanism.
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