The present study was designed to ascertain the in vivo protective efficacy of Ca2+ channel blockers against dermally applied sulphny mustard (SM). Male albino mice were exposed to 1. 5 LD50 of SM (232 mg/kg) percutan...The present study was designed to ascertain the in vivo protective efficacy of Ca2+ channel blockers against dermally applied sulphny mustard (SM). Male albino mice were exposed to 1. 5 LD50 of SM (232 mg/kg) percutaneously and the control group received an equal volume of vehicle (polyethylene glycol 300). Prior to SM application, the animals were administered nifedipine and dextrose saline containing antibiotic by intraperitoneal route. The protection assessed by the mean survival time (MST) was determined by Dunnett's method. The MST was significantly increased in nifedipine treated group.The characteristic biochemical indices of SM intoxication, i. e. lipid peroxidation and reduced glutathione (GSH) were determined in liver from animals sacrificed at 24, 48 and 72 h after exposure. SM application (1 LD50) caused a reduction in GSH level which was restored in nifedipine treated group. SM-induced lipid peroxidation was also prevented by nifedipine administration. The protective effect of nifedipine may be related to its capacity of attenuating SM-induced lipid peroxidation and glutathione depletion展开更多
文摘The present study was designed to ascertain the in vivo protective efficacy of Ca2+ channel blockers against dermally applied sulphny mustard (SM). Male albino mice were exposed to 1. 5 LD50 of SM (232 mg/kg) percutaneously and the control group received an equal volume of vehicle (polyethylene glycol 300). Prior to SM application, the animals were administered nifedipine and dextrose saline containing antibiotic by intraperitoneal route. The protection assessed by the mean survival time (MST) was determined by Dunnett's method. The MST was significantly increased in nifedipine treated group.The characteristic biochemical indices of SM intoxication, i. e. lipid peroxidation and reduced glutathione (GSH) were determined in liver from animals sacrificed at 24, 48 and 72 h after exposure. SM application (1 LD50) caused a reduction in GSH level which was restored in nifedipine treated group. SM-induced lipid peroxidation was also prevented by nifedipine administration. The protective effect of nifedipine may be related to its capacity of attenuating SM-induced lipid peroxidation and glutathione depletion
