RESUMEN
OBJECTIVE: Ionizing radiation interacts with biological systems to induce excessive fluxes of free radicals that attack various cellular components. Melatonin has been shown to be a direct free radical scavenger and indirect antioxidant via its stimulatory actions on the antioxidant system.The aim of this study was to evaluate the antioxidant role of melatonin against radiation-induced oxidative injury to the rat liver after whole body irradiation. MATERIALS AND METHODS: In this experimental study,thirty-two rats were divided into four groups. Group 1 was the control group, group 2 only received melatonin (30 mg/kg on the first day and 30 mg/kg on the following days), group 3 only received whole body gamma irradiation of 10 Gy, and group 4 received 30 mg/kg melatonin 30 minutes prior to radiation plus whole body irradiation of 10 Gy plus 30 mg/kg melatonin daily through intraperitoneal (IP) injection for three days after irradiation. Three days after irradiation, all rats were sacrificed and their livers were excised to measure the biochemical parameters malondialdehyde (MDA) and glutathione (GSH). Each data point represents mean ± standard error on the mean (SEM) of at least eight animals per group. A one-way analysis of variance (ANOVA) was performed to compare different groups, followed by Tukey's multiple comparison tests (p<0.05). RESULTS: The results demonstrated that whole body irradiation induced liver tissue damage by increasing MDA levels and decreasing GSH levels. Hepatic MDA levels in irradiated rats that were treated with melatonin (30 mg/kg) were significantly decreased, while GSH levels were significantly increased, when compared to either of the control groups or the melatonin only group. CONCLUSION: The data suggest that administration of melatonin before and after irradiation may reduce liver damage caused by gamma irradiation.
RESUMEN
Hepatic fibrosis is a common feature in different types of chronic liver injury. The demonstration of the pro-fibrogenesis role of angiotensin II in chronic liver diseases brought up the idea that anti-angiotensin II agents may be effective on improvement of hepatic fibrosis by either blocking the angiotensin II receptor or inhibition of angiotensin converting enzyme (ACE). This study is aimed at comparing the anti-fibrogenesis effects of two ACE inhibitors, captopril and enalapril, in the livers of rats with bile duct ligation through biochemical and histopathological parameters. Male Albino Wistar rats were divided into four groups (n=4-5 each), including sham operated, bile duct ligated, captopril and enalapril treated. After 28 days of treatment, the liver was removed and the levels of hepatic hydroxyproline, glutathione and lipid peroxidation were determined. The degree of the development of fibrosis was evaluated through histopathological numerical scores. The results demonstrated that angiotensin converting enzyme inhibitors increased GSH, decreased lipid peroxidation and improved hepatic fibrosis as shown by histopathology as well as decreased hepatic content of hydroxyproline. Enalapril was significantly more effective than captopril (p<0.001) in improvement of hepatic fibrosis. Also it was shown that enalapril has a significant antioxidative effect (p<0.05) in comparison with captopril. In conclusion, the results of our study suggest that the antifibrotic effect of enalapril may be mostly related to the inhibition of angiotensin converting enzyme.