Background and objectives: toxic liver injury results in nitrooxidative stress. Melatonin is a potent free radical scavenger, an inducible nitric oxide synthase (iNOS) inhibitor and an activator of antioxidant enzymes. The aim of this study was to investigate the hepatoprotective effect of exogenous melatonin on animals with acute toxic hepatitis. Material and methods: 36 healthy Sprague-Dawley male rats were split into three equal groups and given carbon tetrachloride (CCl4), 2 g/kg (CCl4 group) or the same dose of CCl4 and melatonin, 10 mg/kg (CCl4/melatonin group) or saline (control group). The effect of melatonin on prooxidant and antioxidant system indexes, NO and NOS levels in serum and liver, data of mitochondrial chain functions and cytolysis in liver were evaluated in all three groups. Results: melatonin significantly decreased activities of AST, ALT, ceruloplasmine and thiobarbituric acid reactive substance (TBARS) in serum. Catalase activity was lowered in serum but not in the liver. Hepatic TBARS, lipid hydroperoxides and glutathione concentrations were decreased, while superoxide dismutase, mitochondrial cytochrome oxidase and succinate dehydrogenase activities increased. Melatonin inhibited synthesis of stable NO metabolites in serum: NO2-by 37.9%; NO3-by 29.2%. There was no significant difference in content NO2-in the liver, but concentration of NO3-increased by 32.6%. Melatonin significantly reduced iNOS concentrations both in serum (59.7%) and liver (57.8%) but did not affect endothelial isoform enzyme activities neither in serum, nor in liver. The histopathological liver lesions observed in the CCl4/melatonin group were less severe than those seen in the CCl4 group. Conclusions: we demonstrated an ameliorating effect of melatonin on prooxidants and antioxidants, NO-NOS systems balance, mitochondrial function and histopathological lesions in the liver in rats with CCl4-induced hepatitis.
According to the WHO, cancer is the second leading cause of death globally and the third most common cancer is colorectal. A significant etiological factor for carcinogenesis might be oxidative stress. Chemoprevention by consuming natural antioxidants has great perspectives in the struggle to control cancer because it is available and affordable for the wide population. Studies by diverse research groups discovered that grapes, as well as grape-based products, are exceptional sources of the polyphenolic compound resveratrol, which has powerful antioxidant properties. Despite the great number of publications on the anticancer effectiveness of resveratrol, they were all aimed at studying its action once the condition was established. This experiment was the first to study the dynamics of the anticancer activity of resveratrol in the development of chemically induced colorectal cancer. Administrating resveratrol along with 1,2-dimethylhydrazine (DMH) during 30 weeks led to the inhibition of oxidative stress manifestations, in particular, lipid peroxidation. Our research showed that the level of thiobarbituric acid reactive substances in blood serum was 85.1%, 214.6%, and 276.9% lower on the third, fifth, and seventh months of the experiment in the group of rats that obtained resveratrol, compared with the animals affected only by DMH. In the fifth month of the experiment, we noticed that the GPx activity in blood serum was 1.54 times higher than the DMH-control level. During the next 8 weeks, this indicator decreased. The activity of glutathione reductase increased by 2 times in the seventh month, compared with the DMH-control. Histologically resveratrol decelerated the development of the tumor. After 30 weeks of experiment, rats that were receiving only DMH had developed colon adenocarcinoma in situ. In contrast to them, morphological changes in the colon tissue of the animals that obtained resveratrol + DMH could be characterized as signs of mucous colitis.
Features of lipid peroxidation processes and antioxidant system in spleen tissue of white rats in experimental carcinogenesis and application of cytostatics were studied in experimental research. In DMH-induced cancerogenesis it was found a significant increase concentration of TBA-reactive substances and lipid hydroperoxides, decrease of antioxidant enzyme activity and reduced glutathione concentration in the examined organ tissue. The combined use of chemotherapeutic drugs increased imbalance of redox processes in spleen.
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