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Although there are limitations in the extrapolation of animal data directly to humans, animal studies provide an important insight into the mechanisms by which glucosinolates may also exert outcomes in humans

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who suggested that acetaminophen ingestion depletes intracellular GSH stores, which then causes loss of feedback inhibition of γ-glutamylcysteine synthetase activity (Figures 3a and 3b).This increases production of γ-glutamylcysteine, which is partially converted to pyroglutamic acid