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Low levels of glutathione can leave the body vulnerable to oxidative stress and toxin accumulation-factors often linked to chronic inflammation, accelerated aging, and degenerative diseases

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While various risk factors for enhanced APAP toxicity have emerged in the numerous experimental models of steatosis, including induction of Cyp2E1, reduced phase II metabolism, mitochondrial dysfunction, etc., opposite effects have also been described, suggesting that steatosis may not affect toxicity [180]

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