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Using in vitro liver models, we showed that these thiomethyl metabolites are directly linked to the elimination of the hepatotoxic NAPQI metabolites since S-CH 3 -APAP-S and SO-CH 3 -APAP-S are formed at high levels after exposure to NAQPI-derived metabolites (glutathione, cysteine, and mercapturate conjugates) in both primary human hepatocytes and HRG cells

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398 The combination of mitochondrial dysfunction and senescence leads to neuron loss in POLG -related disorders