Taurine and vitamin C influence 8-nitroguanine brain expression following sub-chronic arsenic exposure in the mouse

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-NO_2-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:AS_2O_3,taurine,and vitamin C(Sigma,USA),rabbit polyclonal anti-8-NO_2-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 As_2O_3 group received drinking water containing 4 mg/L AS_2O_3.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 As_2O_3.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-NO_2-G expression in brain tissues was determined by immunohistochemistry. RESULTS:Abnormal,histopathological changes were observed in brain tissue of mice from the As_2O_3 group,which included axonal loss,cell shrinkage,and karyolysis.The above-described changes were minimal in the taurine and vitamin C groups.8-NO_2-G expression was significantly greater in brain tissue from the As_2O_3 group compared with the control group(P<0.05),however, weak 8-NO_2-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.