Such depletion can be due to reduction of GSH due to excessive NAPQI exposure and/or to GSH depletion associated with elevated dopamine secondary to dopamine -hydroxylase inhibition by phenolic Clostridia metabolites
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CYP2R1 expression was not seen in FL83B mouse hepatocytes) and 1--hydroxylase (CYP27B1), along with the increased expression of 24-hydroxylase (CYP24A1), was observed in GSH-deficient hepatocytes
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Research into NAD and its precursors (such as NR and NMN) suggests that restoring NAD availability can support mitochondrial function and metabolic health
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