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The Saccharomyces cerevisiae TEL1 gene is an ortholog of the human ATM ( Ataxia telangiectasia mutated ) gene. S. cerevisiae tel1 mutant ( tel1∆ ) lacking Tel1p, share some of the cellular defects with ATM mutation that includes prevention of oxidative damage repair, premature aging and apoptosis. In the present study, we investigated the protective effects of quercetin on the sensitivity of yeast S. cerevisiae tel1∆ cells exposed to oxidative, apoptotic and DNA damaging stress and viability of tel1∆ cells during chronological aging. Quercetin improved the stress resistance of tel1 ∆ cells when challenged with oxidants such as hydrogen peroxide (H 2 O 2 ), menadine bisulphite (MBS) and tertiary butyl hydroperoxide (t-BHP) by scavenging reactive oxygen species (ROS). Quercetin protected the tel1∆ cells from acetic acid-induced apoptotic cell death and sensitivity against hydroxyurea. We found that quercetin attenuated ROS accumulation and apoptotic markers in tel1∆ cells and therefore an increase in cell viability during chronological aging. Our results from the S. cerevisiae model, suggest that use of quercetin as a food supplement might alleviate oxidative stress mediated DNA damage, apoptosis and age related damaging effects in AT patients and also improve health beneficial effects in humans.

Quercetin enhances stress resistance in Saccharomyces cerevisiae tel1 mutant cells to different stressors