Reeves P G, Rossow K L
United States Department of Agriculture, Grand Forks Human Nutrition Research Center, North Dakota 58202-9034.
Proc Soc Exp Biol Med. 1993 Jul;203(3):336-42. doi: 10.3181/00379727-203-43608.
Zinc (Zn) deficiency causes hypogonadism in a number of different species. Previous work has shown that Zn deficiency reduces the activity of angiotensin-converting enzyme (ACE), a Zn-dependent enzyme, in the testes of prepubertal rats. These studies were designed to determine whether this effect was caused by a change in the concentration of ACE protein. Thirty-five male rats at 26 days of age were divided into three groups. One group was fed ad libitum a Zn-adequate diet (40 mg/kg); another group was fed a similar diet, but deficient in Zn (< 1.0 mg/kg); a third group was pair-fed to the deficient group. After 4 weeks on these regimens, all rats in the ad libitum-fed group and half of the rats in each of the deficient and pair-fed groups were sacrificed, and tissues were collected for analysis. The remaining animals in the Zn-deficient and pair-fed groups were fed a Zn-adequate diet ad libitum for another 2 weeks, then sacrificed. With the use of an enzyme-linked immunosorbent assay for testicular ACE protein, the effect of these treatments on the concentration of ACE protein in testes was determined. After 4 weeks, ACE activity in testes of the Zn-deficient rats was reduced by 74% compared to that in the ad libitum-fed controls. This was accompanied by a 64% reduction in the amount of ACE protein in the testes. There was not a significant effect of pair-feeding. Refeeding Zn-deficient rats a Zn-adequate diet for 2 weeks restored ACE protein concentrations and ACE activity to values not significantly different from those in pair-fed controls. Soluble ACE, but not particulate ACE, of the epididymis was significantly reduced by Zn deficiency. Because the ACE activity of testes has been found primarily in the germinal cells, and soluble ACE in the epididymis is derived from the testes, these findings suggest that the effects of Zn deficiency on testicular and epididymal ACE is caused by an impairment of spermatid development.
锌（Zn）缺乏会导致多种不同物种出现性腺功能减退。先前的研究表明，锌缺乏会降低青春期前大鼠睾丸中血管紧张素转换酶（ACE，一种锌依赖性酶）的活性。这些研究旨在确定这种效应是否由ACE蛋白浓度的变化引起。将35只26日龄的雄性大鼠分为三组。一组随意喂食锌充足的饮食（40毫克/千克）；另一组喂食类似的饮食，但锌含量不足（<1.0毫克/千克）；第三组与缺锌组进行配对喂食。在这些饮食方案实施4周后，随意喂食组的所有大鼠以及缺锌组和配对喂食组中各一半的大鼠被处死，并收集组织进行分析。缺锌组和配对喂食组中剩余的动物再随意喂食锌充足的饮食2周，然后处死。通过使用酶联免疫吸附测定法检测睾丸ACE蛋白，确定了这些处理对睾丸中ACE蛋白浓度的影响。4周后，缺锌大鼠睾丸中的ACE活性与随意喂食的对照组相比降低了74%。与此同时，睾丸中ACE蛋白的量减少了64%。配对喂食没有显著影响。给缺锌大鼠重新喂食锌充足的饮食2周后，ACE蛋白浓度和ACE活性恢复到与配对喂食对照组无显著差异的值。锌缺乏显著降低了附睾中的可溶性ACE，但不影响颗粒性ACE。由于已发现睾丸的ACE活性主要存在于生殖细胞中，且附睾中的可溶性ACE来源于睾丸，这些发现表明锌缺乏对睾丸和附睾ACE的影响是由精子细胞发育受损引起的。
