摘要
BACKGROUND： Arsenic-induced overproduction of reactive nitrogen species results in damage to biomacromolecules in tissues. This is one of major mechanisms of toxic effects due to arsenic. It is assumed that taurine and vitamin C prevent overproduction of peroxynitrite （ONOO） and resist arseniasis by decreasing oxygen-free radical production. OBJECTIVE： To investigate the intervention effects of taurine and vitamin C on 8-nitroguanine （8-NO2-G） expression in the brain of mice exposed to arsenic. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Department of Occupational and Environmental Health, Dalian Medical University, China between March 2007 and July 2008. MATERIALS： As203, taurine, and vitamin C （Sigma, USA）, rabbit polyclonal anti-8-NO2-G antibody and goat anti-rabbit IgG （Dojindo, Japan） were used in this study. METHODS： A total of 40 healthy, Kunming mice were equally and randomly assigned to four groups Mice in the As203 group received drinking water containing 4 mg/L As2O3. Mice in the taurine and vitamin C groups received 150 mg/kg taurine and 45 mg/kg vitamin C, respectively, by gavage, twice per week, and simultaneously received As2O3. Mice in the control group were administered normal drinking water. MAIN OUTCOME MEASURES： Histopathological changes in brain tissues of mice were observed by hematoxylin-eosin staining. 8-NO2-G expression in brain tissues was determined by immunohistochemistry. RESULTS： Abnormal, histopathological changes were observed in brain tissue of mice from the As2O3 group, which included axonal loss, cell shrinkage, and karyolysis. The above-described changes were minimal in the taurine and vitamin C groups. 8-NO2-G expression was significantly greater in brain tissue from the As2O3 group compared with the control group （P 〈 0.05）, however, weak 8-NO2-G expression was observed in the taurine and vitamin C groups. CONCLUSION： Taurine or vitamin C protected against pathological changes and nucleic acid damage due to reactive nitrogen species in brain tissue of mice exposed to arsenic.
BACKGROUND： Arsenic-induced overproduction of reactive nitrogen species results in damage to biomacromolecules in tissues. This is one of major mechanisms of toxic effects due to arsenic. It is assumed that taurine and vitamin C prevent overproduction of peroxynitrite （ONOO） and resist arseniasis by decreasing oxygen-free radical production. OBJECTIVE： To investigate the intervention effects of taurine and vitamin C on 8-nitroguanine （8-NO2-G） expression in the brain of mice exposed to arsenic. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Department of Occupational and Environmental Health, Dalian Medical University, China between March 2007 and July 2008. MATERIALS： As203, taurine, and vitamin C （Sigma, USA）, rabbit polyclonal anti-8-NO2-G antibody and goat anti-rabbit IgG （Dojindo, Japan） were used in this study. METHODS： A total of 40 healthy, Kunming mice were equally and randomly assigned to four groups Mice in the As203 group received drinking water containing 4 mg/L As2O3. Mice in the taurine and vitamin C groups received 150 mg/kg taurine and 45 mg/kg vitamin C, respectively, by gavage, twice per week, and simultaneously received As2O3. Mice in the control group were administered normal drinking water. MAIN OUTCOME MEASURES： Histopathological changes in brain tissues of mice were observed by hematoxylin-eosin staining. 8-NO2-G expression in brain tissues was determined by immunohistochemistry. RESULTS： Abnormal, histopathological changes were observed in brain tissue of mice from the As2O3 group, which included axonal loss, cell shrinkage, and karyolysis. The above-described changes were minimal in the taurine and vitamin C groups. 8-NO2-G expression was significantly greater in brain tissue from the As2O3 group compared with the control group （P 〈 0.05）, however, weak 8-NO2-G expression was observed in the taurine and vitamin C groups. CONCLUSION： Taurine or vitamin C protected against pathological changes and nucleic acid damage due to reactive nitrogen species in brain tissue of mice exposed to arsenic.
基金
the National Natural Science Foundation of China,No.30571584
30600488
