ZINC-DEFICIENCY AFFECTS THE ACTIVITY AND PROTEIN-CONCENTRATION OF ANGIOTENSIN-CONVERTING ENZYME IN RAT TESTES

Zinc (Zn) deficiency causes hypogonadism in a number of different spec ies. Previous work has shown that Zn deficiency reduces the activity o f angiotensin-converting enzyme (ACE), a Zn-dependent enzyme, in the t estes of Prepubertal rats. These studies were designed to determine wh ether this effect was caused by a change in the concentration of ACE p rotein. Thirty-five male rats at 26 days of age were divided into thre e 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 fed group and half of t he 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 libitu m for another 2 weeks, then sacrificed. With the use of an enzyme-link ed immunosorbent assay for testicular ACE protein, the effect of these treatments on the concentration of ACE protein in testes was determin ed. 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. Becaus e the ACE activity of testes has been found primarily in the germinal cells, and soluble ACE in the epididymis is derived from the testes, t hese findings suggest that the effects of Zn deficiency on testicular and epididymal ACE is caused by an impairment of spermatid development .