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The latest researches show that m 6 A is associated with regulating sensitivity of LUAD to ferroptosis

Because GSH is a cofactor for GST isoforms, disruptions in GSH synthesis have the potential to severely disturb the detoxifying capacity of hepatic GSTs (Hardwick et al

N Engl J Med 2004

CYP1A1 metabolism of estrogen, polyaromatic hydrocarbons, and more CYP1A2 metabolism of caffeine, duloxetine, bupropion, aflatoxin B, and more CYP2A6 metabolism of nicotine, coumarin, and more CYP2B6 metabolism of ketamine, methadone, sertraline, and more CYP2C9 metabolism of warfarin, rosuvastatin, celecoxib, and more CYP2C19 metabolism of clopidogrel, some proton pump inhibitors, more CYP2D6 metabolism of some antidepressants, antipsychotics, more CYP3A4 metabolism of half of all prescription drugs CYP2E1 metabolism of fatty acids, alcohol, and some anesthetics Phase II detoxification genes: UGT, GST, Nrf2 Phase II detoxification involves taking the metabolites of phase I and modifying them to be easily excreted through conjugation with sulfur, glutathione, glucuronic acid, amino acids, or methyl groups

[Google Scholar] Sonthalia S, Jha A, Lallas A, Jain G, Jakhar D