Thioaceetamide (standaard)

Thioacetamide (TAA) is an indirect hepatotoxin and causes parenchymal cell necrosis. Thioacetamide requires metabolic activation by microsomal CYP2E1 to thioacetamide-S-oxide initially and then to thioacetamide-S-dioxide, which is a highly reactive metabolite, and its reactive metabolites covalently bind to proteins and lipids thereby causing oxidative stress and centrilobular necrosis. Thioacetamide can induce chronic liver fibrosis, encephalopathy and other events model[1][2][3][4].

62-55-5

12352211

Necroptosis

Apoptosis

Inflammation/Immunology

CC(N)=S

C2H5NS

75.13

[1]Wallace MC, et, al. Standard operating procedures in experimental liver research: thioacetamide model in mice and rats. Lab Anim. 2015 Apr;49 (1 Suppl) :21-9.|[2]Chen IS, et, al. Hepatoprotection of silymarin against thioacetamide-induced chronic liver fibrosis. J Sci Food Agric. 2012 May;92 (7) :1441-7.|[3]Miranda AS, et, al. A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice: a behavioral and neurochemical study. Arq Neuropsiquiatr. 2010 Aug;68 (4) :597-602.|[4]Yeom HJ, et, al. Expression analysis of early response-related genes in rat liver epithelial cells exposed to thioacetamide in vitro. J Vet Med Sci. 2009 Jun;71 (6) :719-27.|[5]Ahmed G Abd Elhameed, et al. Saxagliptin defers thioacetamide-induced hepatocarcinogenesis in rats: A novel suppressive impact on Wnt/Hedgehog/Notch1 signaling. Environ Toxicol Pharmacol|[6]Mohamed E Shaker, et al. Nilotinib counteracts thioacetamide-induced hepatic oxidative stress and attenuates liver fibrosis progression. Fundam Clin Pharmacol. 2011 Apr;25 (2) :248-57.

Room temperature

http://file.medchemexpress.com/batch_PDF/HY-Y0698R/

Reference Standards