Fundamental and Applied Toxicology
Regular ArticleImmunohistochemical Localization of Acetaminophen in Target Tissues of the CD-1 Mouse: Correspondence of Covalent Binding with Toxicity
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Mitochondrial versus microsomal bioactivation of paracetamol by human liver and kidney tissues
2022, Toxicology LettersCitation Excerpt :PAR-induced renal toxicity occurs in the absence of a significant liver toxicity, even in the hepatectomised mice given PAR. In addition, renal protein covalent binding was also observed in-situ (Hart et al., 1994, 1995). Taken together, these data strongly suggested that NAPQI is not transferred from the liver, instead it is formed locally in the kidney.
Acetaminophen and the Developing Lung: Could There Be Lifelong Consequences?
2021, Journal of Pediatrics4-methylpyrazole protects against acetaminophen-induced acute kidney injury
2020, Toxicology and Applied PharmacologyCitation Excerpt :Biomarkers measured in blood from APAP overdose patients also supported this mechanism (McGill et al., 2012a). Our current studies confirmed previous reports (Emeigh Hart et al., 1991; Hart et al., 1994, 1995) that APAP can be metabolized by Cyp2E1 in the kidney forming the reactive metabolite NAPQI, which depletes GSH and form protein adducts. However, hallmarks of APAP-induced liver injury such as mitochondrial protein adduct formation, JNK activation and P-JNK translocation to the mitochondria were not detectable in the kidney at renal subtoxic and toxic doses of APAP.
Pulmonary Irritant Responses: Oxidants and Electrophiles
2018, Comprehensive Toxicology: Third EditionMechanisms of Toxicant-Induced Acute Kidney Injury
2018, Comprehensive Toxicology: Third Edition