维生素E对多柔比星所致生殖毒性雄性大鼠的保护作用

Protective Effect of Vitamin E on Male Rats Submitted to Doxorubicin-induced Testicular Toxicity

目的探讨维生素E对多柔比星致生殖毒性雄性大鼠的保护作用。方法通过一次性静脉注射多柔比星7.5 mg.kg-1制备多柔比星致雄性大鼠生殖毒性损伤模型。维生素E组(n=8)从造模前1 d起,灌服维生素E 100mg.d-1连续14 d。模型组(n=8)造模后,每日经腹腔注射0.9%氯化钠溶液1 mL。对照组(n=8)不造模,每日经腹腔注射0.9%氯化钠溶液1 mL。通过观察大鼠血清超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和睾丸病理组织学变化评估多柔比星对雄性大鼠生殖毒性作用。结果与对照组比较,模型组大鼠血清SOD活性降低,MDA含量升高(P<0.05),睾丸重量和睾丸系数降低(P<0.05),精曲小管生精细胞明显减少,精母细胞和精子细胞退变,部分坏死、脱落。维生素E组大鼠血清SOD活性和MDA含量与对照组比较差异无显著性(P>0.05),睾丸重量和睾丸系数的变化和睾丸病理损伤程度轻于模型组。结论维生素E对多柔比星所致生殖毒性雄性大鼠具有保护作用,其药理作用机制与提高机体抗氧化能力、抑制脂质过氧化反应有关。

Objective To probe into the possible protective effect of vitamin E on male rats submitted to testicular toxicity induced by doxorubicin. Methods The rat model of testicular toxicity was established by a single intravenous injection of 7.5 mg·kg^- of doxorubicin hydrochloride for each animal. Beginning from the day before the establishment of the model, rats of the vitamin E group （n =8） were given each 100 mg·d^-1 of vitamin E by gastmgavage for 14 consecutive days. Animals of the model group （ n = 8） were given each after the establishment of the model an introperutoneal injection of I mL of 0.9% sodium chloride solution q.d. for 14 days. Rats of the control group （ n = 8, not subjected to model establishment） were given each at the same time a daily intraperutioneal injection of I mL of 0.9% sodium chloride solution. The rats were sacrificed 4 weeks later. The testicular toxicity induced by adriamycin was assessed with the measurement of the activities of superoxide dismutase （SOD） and the content of malonyldialdehyde （MDA） in the serum as well as histopathological examination of the testes. Results In comparison with animals of the control group, rats of the model group had lower SOD activities and higher MDA content in the serum （P 〈 0.05 ） as well as a sharp decrease in the absolute and relative testicular weight （ P 〈 0.05 ） associated with a striking reduction of the seminiferous epithelial cells, while the spermatocytes and spermatids were degenerated and a portion of them had undergone necrosis and scaling. In contrast, the difference between rats of the vitamin E group and control group with respect to serum SOD activities and MDA contents was not significant （ P 〉 0. 05 ）, and the changes in the weights of the testes as well as the lesions of seminiferous epithelial cells were trifling in rats of the VE group as compared with those in rats of the model group. Conclusion Vitamin E was shown to exert protective effects on rats submitted to doxorubicin-induced testicular toxicity possibly related to its capability of promoting the antioxidative activity and inhibiting the lipid peroxidation of the organism.