11. Cabreiro F et al
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Alcohol depletes NADPH, induces CYP2E1 (increasing quinone production), and directly damages hepatic Phase II enzymes R Charred and smoked foods are high in polycyclic aromatic hydrocarbons (PAHs) that generate epoxide and quinone intermediates R Cigarette smoke is the single largest source of PAH and benzene exposure, generating massive quinone and epoxide loads R Excess omega-6 fatty acids increase arachidonic acid availability, driving more EET production that sEH then degrades, amplifying the inflammatory cycle R High-dose isolated antioxidants (synthetic vitamin E, synthetic beta-carotene) can paradoxically suppress NRF2 by removing the oxidative signal needed for NRF2 activation R Mold-contaminated environments generate chronic mycotoxin exposure that overwhelms both mEH and NQO1 capacity while simultaneously suppressing NRF2 R Pesticide exposure (organophosphates, organochlorines) generates epoxide intermediates that compete with endogenous substrates for mEH R Plastic-packaged food heated in plastic releases BPA and phthalates that require Phase II metabolism, adding unnecessary load to the system Testing The following lab tests can assess non-conjugation pathway function, cofactor status, and toxic burden
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This suggests that while DSIP improves motor coordination, it may not directly ameliorate the specific asymmetry in motor behavior induced by ketamine in this stroke model
