2010
DOI: 10.1016/j.tiv.2010.06.011
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The toxic effect of thioacetamide on rat liver in vitro

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Cited by 75 publications
(80 citation statements)
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“…Thioacetamide is a strong nephrotoxic substrate [2]. By oxidase system function, thioacetamide is metabolized to its toxic metabolites sulfine (sulfoxide) and sulfene (sulfone) which are then spread in several organs, including plasma, liver, kidney, bone marrow, adrenal and other tissues [9,10].…”
Section: Introductionmentioning
confidence: 99%
“…Thioacetamide is a strong nephrotoxic substrate [2]. By oxidase system function, thioacetamide is metabolized to its toxic metabolites sulfine (sulfoxide) and sulfene (sulfone) which are then spread in several organs, including plasma, liver, kidney, bone marrow, adrenal and other tissues [9,10].…”
Section: Introductionmentioning
confidence: 99%
“…One of these industrial toxins is thioacetamide. This toxin induces hepatic centrilobular necrosis, liver cirrhosis and hepatocellular carcinoma (HCC) 18 . According to the results of this study, the values of albumin, bilirubin,LDH, GGT in groups treated with thioacetamide increased significantly compared to the control and sham1 groups.…”
Section: Resultsmentioning
confidence: 99%
“…We also demonstrated that hepatic total glutathione (the sum of glutathione (GSH) and oxidized form of glutathione, glutathione disulfide (GSSG)) in HFD mice was significantly lower than that in ND mice after TA dosing (Shirai et al, 2013). GSH is a major biological antioxidant (Lu, 1999;Kretzschmar, 1996;Yuan and Kaplowitz, 2009), and it was reported that TA treatment depleted GSH and increased oxida-tive stress in hepatocytes (Staňková et al, 2010). These results and reports suggested that the amount of hepatic GSH and oxidative stress are likely factors for the mechanism of the attenuated TA-induced hepatic necrosis in HFD mice.…”
Section: Introductionmentioning
confidence: 90%