摘要
Aim： To determine the biochemical effect of di-（2-ethylhexyl） phthalate （DEHP） on testes, liver, kidneys and pancreas on day 10 in the process of degeneration of the seminiferous epithelium. Methods： Diets containing 2% DEHP were given to male Crlj：CDI（ICR） mice for 10 days. The dose of DEHP was 0.90±0.52 mg/mouse/day. Their testes, livers, kidneys and pancreata were examined for detection of mono-（2-ethylhexyl） phthalate （MEHP）, nitrogen oxides （NOx） produced by peroxidation of nitric oxide （NO） with free radicals, and lipid peroxidation induced by the chain reaction of free radicals. Results： Histological observation and serum analysis showed the presence of severe sperrnatogenic disturbance, Leydig cell dysfunction, liver dysfunction and dehydration. Unexpectedly, the concentration of MEHP in the testes was extremely low compared with that in the liver. However, the concentration of the NOx in the testes was as high as the hepatic concentration. Furthermore, free radical-induced lipid peroxidation was histochemically detected in the testes but not in the liver. Conclusion： The results indicate that DEHP-induced aspermatogenesis is caused by the high sensitivity of the testicular tissues to MEHP rather than the specific accumulation or uptake of circulating MEHP into the testes.
Aim： To determine the biochemical effect of di-（2-ethylhexyl） phthalate （DEHP） on testes, liver, kidneys and pancreas on day 10 in the process of degeneration of the seminiferous epithelium. Methods： Diets containing 2% DEHP were given to male Crlj：CDI（ICR） mice for 10 days. The dose of DEHP was 0.90±0.52 mg/mouse/day. Their testes, livers, kidneys and pancreata were examined for detection of mono-（2-ethylhexyl） phthalate （MEHP）, nitrogen oxides （NOx） produced by peroxidation of nitric oxide （NO） with free radicals, and lipid peroxidation induced by the chain reaction of free radicals. Results： Histological observation and serum analysis showed the presence of severe sperrnatogenic disturbance, Leydig cell dysfunction, liver dysfunction and dehydration. Unexpectedly, the concentration of MEHP in the testes was extremely low compared with that in the liver. However, the concentration of the NOx in the testes was as high as the hepatic concentration. Furthermore, free radical-induced lipid peroxidation was histochemically detected in the testes but not in the liver. Conclusion： The results indicate that DEHP-induced aspermatogenesis is caused by the high sensitivity of the testicular tissues to MEHP rather than the specific accumulation or uptake of circulating MEHP into the testes.
