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It is conceivable that this general mechanism can explain Mercury-induced oxidative stress not only through a continuous depletion of the reduced glutathione pool, but also by interfering with enzymes operating through active sites based on vicinal thiol groups or which are regulated by glutathionylation of sensing cysteine residues

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Nonsteroidal anti-inflammatory drugs (NSAIDs) also act through the COX pathway, which accounts for similar analgesic and antipyretic effects

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Renal response to tissue injury: lessons from heme oxygenase-1 GeneAblation and expression

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