Role of mammalian cytosolic molybdenum Fe–S flavin hydroxylases in hepatic injury

Chloroform-induced oxidative stress in rat liver: Implication of metallothionein

“…Intraperitoneal administration of CHCl 3 augmented lipid peroxidation up to fourfold in mice liver (Skrzypińska et al, 1991). Ali et al (2008) also reported an important increase of MDA in hepatic tissue of rats treated ip with a lethal dose of CHCl 3 (1500 mg/kg). Although we recorded a slight but statistically significant increase of MDA in 24-and 48-hour groups, only at the non-cytotoxic dose (150 mg/kg) of this halomethane.…”

“…Cellular GSH concentrations are an important determinant of susceptibility, and perturbations of glutathione homeostasis may affect markedly the toxicity of CHCl 3 ( IPCS, 1994). Conflicting results about the impact of CHCl 3 on GSH depletion in rodents were reported with either high doses (Ali et al, 2008;Docks and Krishna, 1976) or low ones (Di Consiglio et al, 2001;Gemma et al, 1996). Several studies support the view that GSH depletion occurred in association with cytotoxicity.…”

Dried peel fraction of Citrus sinensis partially reverses pathological changes in rat model of liver cirrhosis

“…In this study, we provide substantial and convincing evidence suggesting the therapeutic effect of an aqueous-alcoholic extract of dried orange peels in animal model of liver cirrhosis. Thioacetamide induces hepatic injury by various mechanisms [17,[36][37][38], and produces various forms of 'a 1 ' indicates the limonene standard, 'a 2 ' the limonene in the extract, 'b 1 ' is the peak of b-sitosterol standard, 'b 2 ' is b-sitosterol in the extract, 'c 1 ' is the ascorbic acid standard, and 'c 2 ' is the ascorbic acid in the extract. Comparison of standards and peaks confirmed limonene, b-sitosterol, and ascorbic acid in the test fraction liver diseases depending on the dosage and duration of administration: higher dose produce necrosis [39], fulminant hepatic failure, and early death [40], whereas lower doses administered over a prolonged period of time culminates in liver fibrosis/cirrhosis [41] and hepatocellular carcinoma [42].…”

“…Hepatic tissue was subjected to further biochemical analysis. The procedure for the preparation of sample and subcellular fractionation was similar to the one described in one of our earlier publications [17]. Serum aminotransferases [18], alkaline phosphatase [19], and hepatic c-glutamyl transferase [20], Fig.…”

“…1 Schematic illustration of the treatment protocol design to induce liver cirrhosis and study the effect of test fraction in rat. Following the completion of 16 weeks treatment with thioacetamide, rats were left untreated for 1 week to ensure that the thioacetamide or its metabolites are eliminated and the constituents in the extract do not interfere with the metabolites or the drug metabolizing system [17] lipid peroxidation [21], reduced glutathione [22], glutathione reductase [23], glutathione peroxidase [24], and catalase [25] were measured in all groups. Selected Phase I and Phase II drug metabolizing enzymes, xanthine oxidase [26] and glutathione s-transferase [27] were also measured in the post-mitochondrial supernatant.…”