Gamal H. El-Sokkary1. 1. Department of Zoology, Faculty of Science, Assiut University, Assiut, 71516 Egypt. EL-SOKKARY@USA.NET
Abstract
OBJECTIVES: Free radical scavengers can protect against the genotoxicity induced by chemical carcinogens by decreasing oxidative stress. The protective effect of the antioxidant melatonin was studied in the kidney and liver of rats treated with the kidney-specific carcinogen potassium bromate (KBrO(3)). The major endpoint of oxidative damage measured in this report was lipid peroxidation. METHODS: Four groups of male rats (controls, melatonin-injected [10 mg/kg x4], KBrO(3)-injected [100 mg/kg], and melatonin+-KBrO(3)) were used in the current study. The concentrations of malondialdehyde (MDA) were assayed as an index of oxidatively damaged lipid in the kidney and liver. RESULTS: Twenty-four hours after KBrO(3) administration, MDA levels were significantly increased in the kidney while the increase in the liver was not statistically significant compared to levels in control rats. The percentage increases in lipid peroxidation products were 32.8% and 12.6% for the kidney and liver, respectively. In rats given melatonin 30 minutes before KBrO(3), and three more times after KBrO(3) (i.e., every 6 hours), the increase in MDA levels was reduced in the kidney. Histopathological examination demonstrated marked changes in the structure of the kidney and slight changes in the liver. In the kidney, microscopic examination revealed atypical tubules, atypical hyperplasia, hyaline droplet degeneration, necrotic changes and stratified squamous cell metaplasia. Again, melatonin treatment inhibited the tissue damage associated with KBrO(3) administration. CONCLUSION: These results show that melatonin as an antioxidant and free radical scavenger can prevent oxidative stress induced by the carcinogen KBrO(3).
OBJECTIVES:Free radical scavengers can protect against the genotoxicity induced by chemical carcinogens by decreasing oxidative stress. The protective effect of the antioxidant melatonin was studied in the kidney and liver of rats treated with the kidney-specific carcinogen potassium bromate (KBrO(3)). The major endpoint of oxidative damage measured in this report was lipid peroxidation. METHODS: Four groups of male rats (controls, melatonin-injected [10 mg/kg x4], KBrO(3)-injected [100 mg/kg], and melatonin+-KBrO(3)) were used in the current study. The concentrations of malondialdehyde (MDA) were assayed as an index of oxidatively damaged lipid in the kidney and liver. RESULTS: Twenty-four hours after KBrO(3) administration, MDA levels were significantly increased in the kidney while the increase in the liver was not statistically significant compared to levels in control rats. The percentage increases in lipid peroxidation products were 32.8% and 12.6% for the kidney and liver, respectively. In rats given melatonin 30 minutes before KBrO(3), and three more times after KBrO(3) (i.e., every 6 hours), the increase in MDA levels was reduced in the kidney. Histopathological examination demonstrated marked changes in the structure of the kidney and slight changes in the liver. In the kidney, microscopic examination revealed atypical tubules, atypical hyperplasia, hyaline droplet degeneration, necrotic changes and stratified squamous cell metaplasia. Again, melatonin treatment inhibited the tissue damage associated with KBrO(3) administration. CONCLUSION: These results show that melatonin as an antioxidant and free radical scavenger can prevent oxidative stress induced by the carcinogen KBrO(3).