TOXIC EFFECTS OF 1,2-DIBROMO-3-CHLOROPROPANE ON THE UROGENITAL SYSTEM

1，2-二溴-3-氯丙烷(DBCP)能迅速降低 急性暴露后实验动物的雄性生育能力。研究 以确定这一现象的生化基础 效果。DBCP处理大鼠7天后引起的小鼠 同种异体精子中葡萄糖代谢为二氧化碳的能力下降， 伴随而来的是乳酸积累的增加。这些 结果表明，DBCP对精子碳水化合物有抑制作用 糖酵解后部位的新陈代谢。DBCP类似地被禁止 多种三元酸循环的代谢 费希尔附睾精子中CO_2的中间体 344只大鼠。DBCP不抑制NAD依赖酶的活性 糖酵解或三元酸中的脱氢酶 循环；然而，它确实抑制了氧气消耗的速度 来自内源底物和NAD连接的三羧酸 中间体。氧化琥珀酸酯，一种FAD连接的底物， 对DBCP不敏感。结论：DBCP对小鼠的生长发育有抑制作用 精子NADH脱氢酶阶段的碳水化合物代谢 在线粒体的电子传递链中。抑制 DBCP的碳水化合物代谢归因于亲本 化合物，因为所有的影响都是即刻的，并且与时间呈线性关系。 接触对苯二酚引起的快速不孕可能是 细胞内的ATP水平低于所需的 精子对卵子的运动或穿透。

1,2-Dibromo-3-chloropropane (DBCP) produces a rapid decrease in male fertility in laboratory animals after acute exposure. Studies were performed to determine the biochemical basis for this effect. Treatment of rats with DBCP for seven days caused a decrease in the metabolism of glucose to CO2 in isoplated sperm, with a concomitant increase in lactate accumulation. These results indicate that DBCP may inhibit sperm carbohydrate metabolism at a site post-glycolysis. DBCP similarly inhibited the metabolism of a variety of tricarboxylic acid cycle intermediates to C02 in epididymal sperm isolated from Fischer 344 rats. DBCP did not inhibit the activities of NAD-dependent dehydrogenase enzymes in glycolysis or the tricarboxylic acid cycle; however, it did inhibit the rates of oxygen consumption from endogenous substrates and NAD-linked tricarboxylic intermediates. Oxidation of succinate, an FAD-linked substrate, was insensitive to DBCP. It is concluded that DBCP inhibits sperm carbohydrate metabolism at the NADH dehydrogenase step in the mitochondrial electron transport chain. Inhibition of carbohydrate metabolism by DBCP was attributed to the parent compound, since all effects were immediate and linear with time. The rapid infertility caused by exposure to DBCP may be a result of cellular ATP levels being less than that which is required for motility or penetration of the ovum by the sperm.