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On the other hand, it is known that mitochondrial production of oxygen-derived radicals is increased with exercise [4], and this fact could be a major mechanism for the exercise-related increase in oxidative stress

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Caspase-3, an important regulator of apoptotic responses, can undergo glutathionylation, leading to the inactivation of caspase-3 by GSSG in a dose- and time-dependent manner [25], suggesting that apoptosis can be regulated by glutathionylation

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