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Therefore, in both mammalian and yeast cells, the response to an increase in oxidative stress is an elevation of the levels of glutathione, which can be used to eliminate ROS and facilitate native disulphidebond formation

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The implication of this self-perpetuating cycle is that oxidative stress is not merely a bystander but an active driver of OA progression, creating a feed-forward loop where inflammation begets more oxidative stress, and vice versa

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