Reactive oxygen species (ROS) are cytotoxic agents that lead to significant oxidative damage. Bisphenol A (BPA) is a contaminant with increasing exposure to it and exerts both toxic and estrogenic effects on mammalian cells. Due to limited information concerning the effect of BPA on liver, this study investigates whether BPA causes hepatotoxicity by induction of oxidative stress in liver. Rats were divided into five groups: The first four groups, BPA (0.1, 1, 10, 50 mg/kg/day) were administrated orally to rats for four weeks. The fifth group was taken water with vehicle. The final body weights in the 0.1 mg group showed a significant decrease compared to control group. Significant decreased levels of reduced glutathione, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and catalase activity were found in the 50 mg BPA group compared to control groups. High dose of BPA (50 mg/kg) significantly increased the biochemical levels of ALT, ALP and total bilirubin. BPA effect on the activity of antioxidant genes was confirmed by real time PCR in which the expression levels of these genes in liver tissue were significantly decrease compared to control. Data from this study demonstrate that BPA generate ROS and reduce the antioxidant gene expression that causes hepatotoxicity.

The active constituent profile in Cape gooseberry (Physalis peruviana L.) juice was determined by GC-MS. Quercetin and kaempferol were active components in the juice. In this study we have evaluated its potential protective effect on hepatic injury and fibrosis induced by carbon tetrachloride (CCl4). Twenty-eight rats divided into 4 groups: Group I served as control group, and Group II received weekly i.p. injection of 2 mL CCl4/kg bwt for 12 weeks. Group III were supplemented with Physalis juice via the drinking water. The animals of Group IV received Physalis juice as Group III and also were intraperitoneally injected weekly with 2 mL CCl4/kg bwt for 12 weeks. Hepatoprotective effect was evaluated by improvement in liver enzymes serum levels, reduction in collagen areas, downregulation in expression of the fibrotic marker MMP-9, reduction in the peroxidative marker malonaldehyde and the inflammatory marker nitric oxide, and restoration of the activity of antioxidant enzymatic and nonenzymatic systems, namely, glutathione content, superoxide dismutase, catalase, glutathione-S-transferase, glutathione peroxidase, and glutathione reductase activities. The results show that the potential hepatoprotective effects of Physalis peruviana may be due to physalis acts by promotion of processes that restore hepatolobular architecture and through the inhibition of oxidative stress pathway.

Asian Pacific J Cancer Prev, 13 (11), [5405][5406][5407][5408] IntroductionLiver is the main organ involved in gluconeogenesis and in production and transportation of fatty acids and cholesterol in which its metabolic disease is prerequisited for cancer. Tissue fibrosis is a major cause of dysfunction in the hepatic systems (Glass et al., 2011). Hepatic fibrosis is influenced by several epigenetic factors that control the wound-healing response. Fibrosis is the excess deposition of extracellular matrix (ECM) components resulted from an imbalance of ECM molecule metabolism (Jiang et al., 2010; Glass et al., 2011) either by an increased synthesis or decreased degradation of ECM components or both. Collagens are synthesized by mesenchymal cells including fibroblasts and have an important role in the development of fibrosis (Jiang et al., 2010). MiRNAs are the smallest, non-coding RNA, plays important roles in post-transcriptional regulation (Borchert et al., 2006). In the nucleus, the miRNA genes are transcribed as primarymiRNA molecules, next processed forming pre-miRNAs (Lee et al., 2004; Borchert et al., 2006), finally transported to the cytoplasm for further processing (Lee et al., 2003; Lund et al., 2004

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