Stallard L, Reeves P G
Agricultural Research Service, United States Department of Agriculture, Grand Forks Human Nutrition Research Center, ND 58202-9034, USA.
J Nutr. 1997 Jan;127(1):25-9. doi: 10.1093/jn/127.1.25.
Zinc deficiency results in reduced testicular angiotensin-converting enzyme (ACE) activity and reduced amounts of ACE protein in the testes of young rats. In the present study, we examined the effect of zinc deficiency on the relative abundance of testicular ACE mRNA and its relationship to ACE activity over time. Forty-five male rats at 7 wk of age were placed on one of three feeding regimens: 1) a diet adequate in zinc, 2) a diet deficient in zinc and 3) a diet adequate in zinc that was fed in an amount equal to that consumed by a paired mate fed the zinc-deficient diet. Rats were killed after 3, 5 and 7 wk. Rats fed the zinc-deficient diet had significantly lower (P < 0.01) body weight gain and testis weight at each week sampled than the other groups. They also showed compromised zinc status as evidenced by significantly lower (P < 0.01) serum and testis zinc concentrations. At each period, rats fed the zinc-deficient diet had significantly lower (P < 0.01) testicular ACE activity than rats fed either of the zinc-adequate diets. Coinciding with low ACE activity, there was a lower (P < 0.01) relative abundance of ACE mRNA in the group for the zinc-deficient diet than in either of the zinc-adequate groups. The results suggest that much of the low ACE activity in the testis of rats in the latter stages of zinc deficiency is attributable to a reduction in ACE gene transcription. However, an effect of the deficiency on ACE mRNA turnover is not ruled out.