US EPA

6793209 

Journal Article 

Review 

Possible Pathways of Hepatotoxicity Caused by Chemical Agents 

dos Santos, KM; Tsuji, SS; Saraiva Camara, M; Michereff, SJ; Mohi-Ud-din, R; Mir, RH; Sawhney, G; Dar, MA; Bhat, Z; , 

2019 

Yes 

Current Drug Metabolism
ISSN: 1389-2002
EISSN: 1875-5453 

BENTHAM SCIENCE PUBL LTD 

SHARJAH 

20 

11 

867-879 

English 

31702487 

10.2174/1389200220666191105121653 

WOS:000504877500002 

Background: Liver injury induced by drugs has become a primary reason for acute liver disease and therefore posed a potential regulatory and clinical challenge over the past few decades and has gained much attention. It also remains the most common cause of failure of drugs during clinical trials. In 50% of all acute liver failure cases, drug-induced hepatoxicity is the primary factor and 5% of all hospital admissions.Methods: The various hepatotoxins used to induce hepatotoxicity in experimental animals include paracetamol, CCl4, isoniazid, thioacetamide, erythromycin, diclofenac, alcohol, etc. Among the various models used to induce hepatotoxicity in rats, every hepatotoxin causes toxicity by different mechanisms.Results: The drug-induced hepatotoxicity caused by paracetamol accounts for 39% of the cases and 13% hepatotoxicity is triggered by other hepatotoxic inducing agents.Conclusion: Research carried out and the published papers revealed that hepatotoxins such as paracetamol and carbon-tetrachloride are widely used for experimental induction of hepatotoxicity in rats. 

Cytochrome P450; Hepatotoxicity; Hepatotoxins; Lipopolysaccharide; Liver damage; Liver toxicity; Xenobiotics; aflatoxin B1; alcohol; azathioprine; carbon tetrachloride; caspase 9; chemical agent; cyclosporine; cytochrome P450; cytochrome P450 2E1; diclofenac; doxorubicin; erythromycin; galactosamine; glutathione; glutathione peroxidase; glutathione reductase; glycogen synthase kinase 3; halothane; isoniazid; lead; microcystin; mitogen activated protein kinase p38; paracetamol; phenytoin; ranitidine; reactive oxygen metabolite; superoxide dismutase; thioacetamide; valproic acid; acute kidney failure; acute liver failure; AMPK signaling; carcinogenesis; CD4+ T lymphocyte; cytotoxicity; human; immune response; inflammatory bowel disease; JAK-STAT signaling; liver cirrhosis; liver injury; liver toxicity; MAPK signaling; Microcystis; nephrotoxicity; nonhuman; phase 1 clinical trial (topic); Pi3K/Akt signaling; protein phosphorylation; Review; risk factor; signal transduction; TGF beta signaling; toxic hepatitis; animal; liver; liver disease; metabolism; Animals; Chemical and Drug Induced Liver Injury; Humans; Liver; Liver Diseases