Autoantibodies against Cytochromes P450: Role in Human Diseases
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Cytochrome P450 endoplasmic reticulum-associated degradation (ERAD): therapeutic and pathophysiological implications
2020, Acta Pharmaceutica Sinica BCYP2E1 autoantibodies in liver diseases
2014, Redox BiologyCitation Excerpt :From these observations, subsequent studies have implicated immunity against hepatic CYPs in idiosyncratic adverse reactions to drugs and in autoimmune hepatitis. In particular, antibodies against different CYP isoforms were detected in the case of dihydralazine- (anti-CYP1A2) or tienilic acid- (anti-CYP2C9) induced hepatitis as well as during hypersensitivity reactions to the aromatic anti-convulsants (anti-CYP3A) or in children treated with immunosuppressive drugs (CYP3A4, CYP2C9) [5–9]. The relevance of these observations in relation to the pathogenesis of drug-induced hepatitis was supported by the demonstration of that several functional CYP isoforms are transported from the Golgi apparatus via the secretory vesicles [10] to the plasma membrane of hepatocytes, where they and can be targeted by anti-CYP antibody [11,12].
Mechanisms of drug toxicity and relevance to pharmaceutical development
2011, Drug Metabolism and PharmacokineticsAutoimmune Models
2010, Comprehensive Toxicology, Second EditionEvidence for cellular protein covalent binding derived from styrene metabolite
2010, Chemico-Biological InteractionsCitation Excerpt :The documented blood protein adduction suggested the possibility that there are cellular protein adducts derived from styrene metabolites and encouraged us to investigate the correlation between styrene-derived cellular protein adduction and styrene toxicity. Covalent modification of specific proteins can activate the immune system to cause an autoimmune response [22,23]. It might also disrupt the protein function or cause cell death by disrupting some regulatory pathway [23,24].
Biochemical Mechanisms of Drug Toxicity
2007, Principles of Clinical Pharmacology