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Effects of Ferro Sulphate and Carbon Tetracholide in Liver of Rat
Ferro sulphate (FeSO.) overload and carbon tetrachloride (Gel.) are chemical hepatacarcinogen. Ferro sulphate disrupts the redox balance of the cell and generates chronic oxidative stress by which modulates signaling networks related to malignant transformation. Meanwhile ecl. induces hepatic damage in lipid peroxidation and decreases activities of antioxidant enzymes and generation of free radicals. The aim of this study is to investigate the effect of a pause of chemical hepatocarcinogen induced in Rattus norvegicus rats. Two months old adult male Rattus norvegicus rats weighing around 110-191 g were used. The rats were divided into three groups. In group I (n = 3), no-treatment control; in group 11 (n = 31, rats were fed 3.5% FeSO, in the diet together with 0.1 ml/ kgBW eCI, administered by gavage per os 5 days a week for 3 weeks. However, in group III (n = 3), rats were administered by chemical hepatocarcinogen like group I then continued with no-treatment for 2 weeks (a pause of 2 weeks was inserted). Body weight were determined per week. At the end of the experiment, rats were fasted overnight, and then 3.0 ml of blood was drawn from the rats from the vena orbital is in EDTA-tube and then sacrificed. Liver and body weight of rats were determined for each group. Plasma was prepared to biochemical estimation of different parameters like total protein (TP), non-functional plasma enzymes: aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma glutamyl transferase (gGT) by biochemical test kits in SYNCHRON CX® System(s). The liver tissue was used for histological and immunohistochemical assessment. All data were analyzed with one-way ANOVA, p < 0.05 for the statistical comparison of groups in Matrix Laboratory (MATLAB) programs in Microsoft Windows XP. According to the research results of the body weight on treated group gained significantly less body weight than control group (p = 0.00). Liver weight at the end of the experiment were significantly decreased in treated group compared to control (p = 0.00); but Liver! Body weight ratio were significantly increased in treated group compared to control (p=O.OO). The blood plasma were significant differences in the values of TP and gGT (p = 0.00 and 0.00), but the values of AST, ALT, and ratio of AST to AL T were not significant differences (p = 0.62,0.67, and 0.26 respectively). Histopathological studies of the liver section of treated group showed the damage of the liver cells. In the group of a pause of chemical hepatocarcinogen induced in rats were no major morphological changes were observed compared to group that administered for 3 weeks, except for decreased steatosis level. An overall decrease in vacuoles at the group of a pause suggested a change metabolism and toxin depletion over time. Furthermore, p53 immunohistochemistry on 9 cases revealed no p53 mutations or protein overexpression. It was concluded that p-53 mutation was not detected i~ Rattus norvegicus rats that induced hepatocarcinogenic agent FeSO, 3.5% and CCI, 0.1 ml/ kg BW for 3 weeks and hepatic injury still encountered in a pause of chemical hepatocarcinogen induced showed that the recovery was not complete.
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