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Volumn 215, Issue 1, 2012, Pages 40-41

Caveats of using acetaminophen hepatotoxicity models for natural product testing

Author keywords

Acetaminophen; Hepatotoxicity; HepG2 cells; Mitochondria; Protein adducts; Reactive metabolites

Indexed keywords

DIOSCIN; GLUTATHIONE; NATURAL PRODUCT; PARACETAMOL; PEROXYNITRITE; STRESS ACTIVATED PROTEIN KINASE; UNCLASSIFIED DRUG;

EID: 84867606870     PISSN: 03784274     EISSN: 18793169     Source Type: Journal    
DOI: 10.1016/j.toxlet.2012.09.023     Document Type: Letter
Times cited : (12)

References (14)
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  • 4
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    • Current issues with acetaminophen hepatotoxicity - a clinically relevant model to test the efficacy of natural products
    • Jaeschke H., McGill M.R., Williams C.D., Ramachandran A. Current issues with acetaminophen hepatotoxicity - a clinically relevant model to test the efficacy of natural products. Life Sciences 2011, 88:737-745.
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    • Oxidant stress, mitochondria, and cell death mechanisms in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity
    • Jaeschke H., McGill M.R., Ramachandran A. Oxidant stress, mitochondria, and cell death mechanisms in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity. Drug Metabolism Reviews 2012, 44:88-106.
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    • Mitochondrial permeability transition in acetaminophen-induced necrosis and apoptosis of cultured mouse hepatocytes
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  • 8
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    • N-acetylcysteine does not protect HepG2 cells against acetaminophen-induced apoptosis
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    • The mechanism underlying acetaminophen-induced hepatotoxicity in humans and mice involves mitochondrial damage and nuclear DNA fragmentation
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* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.