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The connection between the elevation of this organic acid and acetaminophen use was first reported by Pitt et al., 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).40 This increases production of γ-glutamylcysteine, which is partially converted to pyroglutamic acid