Pant N, Shankar R, Srivastava S P
Industrial Toxicology Research Centre, Lucknow, India.
Hum Exp Toxicol. 1997 May;16(5):267-72. doi: 10.1177/096032719701600506.
Male offspring of adult females treated with 0.2 or 0.4 mg/kg during either the whole of pregnancy or the whole of the lactation period did not induce generalised toxic effects. A significant alteration in enzymatic activities i.e. SDH (decreased), LDH and Y-GT (increased) were observed in testes only at 0.4 mg/kg. A decrease in sperm motility, sperm count along with increase in percent abnormal sperm was observed at 0.4 mg/kg dose level. Histopathological examination revealed loss of spermato-genesis, degenerative changes in Sertoli cells which are well supported with biochemical studies indicating that carbofuran interferes with the maturation process of testis. No such effects were observed at 0.2 mg/kg. The testicular and spermatotoxic effects observed in rats given in utero or lactational exposure may be due to transfer of carbofuran or its metabolites through placenta or mothers milk.
在整个孕期或整个哺乳期接受0.2或0.4毫克/千克剂量处理的成年雌性大鼠所产雄性后代未出现全身性毒性作用。仅在0.4毫克/千克剂量时,睾丸中的酶活性出现显著改变,即琥珀酸脱氢酶(SDH)活性降低,乳酸脱氢酶(LDH)和γ-谷氨酰转移酶(Y-GT)活性增加。在0.4毫克/千克剂量水平下,观察到精子活力下降、精子数量减少以及异常精子百分比增加。组织病理学检查显示精子发生丧失,支持细胞出现退行性变化,生化研究有力地证明了克百威会干扰睾丸的成熟过程。在0.2毫克/千克剂量时未观察到此类影响。在子宫内或哺乳期接触克百威的大鼠中观察到的睾丸和精子毒性作用可能是由于克百威或其代谢产物通过胎盘或母乳转移所致。