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Although initial studies suggested that GSH depletion was only a byproduct of oxidative stress generated during cell death, recent discoveries suggest that GSH depletion and post-translational modifications of proteins through glutathionylation are critical regulators of apoptosis

The inhibition of pyrogallol oxidation by SOD was monitored and the amount of enzyme producing 50% inhibition was defined as one unit of enzyme activity

This process cannot take place without adequate levels of glutathione

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