摘要
用0.01、0.10、1.00 mg.L-1久效磷暴露金鱼21 d,测定了精巢乳酸脱氢酶(LDH)、酸性磷酸酶(ACP)、碱性磷酸酶(ALP)的活性,并观察了精巢显微和超微结构的变化。结果表明:久效磷暴露21 d,精巢小叶基膜断裂,Leydig氏细胞水肿,小叶间质扩大,支持细胞核膜溶解,胞质内脂滴和髓磷脂象数量增多。1.00 mg.L-1久效磷造成了生殖腺指数的显著下降,对精巢发育有一定程度的延迟作用。随着久效磷暴露浓度的升高,LDH,ACP,ALP的活性逐渐下降,0.10、1.00 mg.L-1久效磷暴露组精巢LDH,ACP的活性下降显著,而各暴露组的精巢ALP活性呈现不显著下降趋势。推测久效磷可能通过损伤精巢超显微结构和降低LDH,ACP和ALP活性,干扰精巢能量代谢,造成对雄性金鱼的生殖毒性。
After 21 days' exposure of adult male goldfish( Carassius auratus) to monocrotophos (0.01, 0.10,1.00 mg · L^-1), we measured activities of lactate dehydrogenase(LDH), acid phosphatase( ACP), alkaline phosphatase (ALP) in testis and observed micro-ultrastructure of testis by light and electron microscopy separately. It was found that the gonado-somatic (GSI) decreased significantly, ground membrane dissolved, Leydig' s cell swelled and interstitial tissue enlarged, as a result of exposure to monocrotophos at the concentration of 1.00 mg · L^-1. Monocrotophos induced dissolution of nuclear membrane of the Sertoli' s cell, and the increase of lipid droplet and myelin-like figure number in Sertoli' s cell. The activities of LDH, ACP and ALP in testis decreased gradually, as the exposure concentration of monocrotophos increased. Exposure to monocrotophos at concentrations of 0.10 and 1.00 mg · L^-1 resulted in the decrease of LDH and ACP activities in testis. However, the ALP activity did not decrease significantly at various exposure concentrations. It is supposed that the energy metabolism was interrupted as a result of the changes of micro-ultrastructure and the decrease of LDH, ACP, ALP activities in goldfish testis, which caused the reproductive toxicity effect.
出处
《水产学报》
CAS
CSCD
北大核心
2007年第5期568-574,共7页
Journal of Fisheries of China
基金
国家自然科学基金资助项目(30671618)
关键词
金鱼
久效磷
乳酸脱氢酶
磷酸酶
超微结构
精巢
goldfish
monocrotophos
lactate dehydrogenase (LDH)
phosphatase
ultrastructure
testis