The response of to oxidative stresses has been examined. On challenging for 60 min at early exponential phase with either 40 mM HO or 6 mM menadione (MD), a superoxide-generating agent, less than 10% of the cells survived. Pretreating cells with 0.2 mM HO or 0.2 mM MD for 1 h significantly increased survival of these lethal doses of each oxidant, indicating the existence of an adaptive response to oxidative stress. Furthermore, cells pretreated with a low dose of MD became resistant to a lethal dose of HO. However, cells pretreated with HO became only partially resistant to a lethal dose of MD. Adaptation was accompanied by the induction of several oxidative defence enzymes. The presence of 0/2 mM HO induced catalase by 2.8-fold and peroxidase by 2.0-fold. The presence of 0.2 mM MD induced catalase by 2.0-fold, glucose-6-phosphate dehydrogenase by 1.9-fold, glutathione reductase by 2.7-fold, peroxidase by 3.0-fold, and superoxide dismutase (SOD) by 2.1-fold. The higher induction of these defence enzymes by MD may explain why MD-pretreated cells were better adapted to lethal doses of oxidants than HO-pretreated ones. All these enzymes except SOD and peroxidase increased more than 5.0-fold as cells proceeded into stationary phase. The GSH/GSSG ratio also increased by 60%. These changes accord with the observation that stationary phase cells survive oxidant treatment better than cells in vegetative growth.


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