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Abstract Oxidative stress is an important regulator of the mammalian epigenome, with redox imbalances triggering stress-responsive epigenetic modifications linked to various diseases
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Rapid acetylators were competent in isoniazid acetylation but the drug was cleared less efficiently in the slow acetylator group, which resulted in elevated serum concentration and led to adverse neurologic side effects due to an accumulation of unmetabolized drug (Brockton et al., 2000)
2015;5: a022426
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