Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 10, 1996
Publication Date: N/A
Interpretive Summary: Zinc (Zn) is an essential mineral nutrient required in the diet. A deficiency of Zn causes a failure in the development of sperm in the testes in a number of different species including the human. There is a possibility that this effect is caused by the failure of some important reaction that requires Zn. There is an enzyme called angiotensin converting enzyme (ACE) that requires Zn for optimal function. This enzyme increases in activity as the testes mature and is depressed in the testes of rats that are fed a Zn-deficient diet. Since the manufacture of an enzyme is controlled by specific genes, it is important to know if the depression in activity of ACE by zinc deficiency is regulated in this way. This experiment showed that this may be the case. When adult rats were fed zinc-deficient diets, the activity of the enzyme and the amount of ACE mRNA, the component made from the gene that in turn makes ACE protein, was significantly less than that of rats fed zinc-adequate diets. This type of information could possibly be used in future studies to determine the dietary requirement of Zn for the maintenance of sperm count and activity in adult men.
Technical Abstract: Zinc deficiency results in reduced testicular angiotensin converting enzyme (ACE) activity and reduced amounts of ACE protein in the testes of young rats. We examined how zinc deficiency affects ACE mRNA expression 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, (+)Zn; 2) a diet deficient in zinc, (-)Zn; and 3) a diet adequate in zinc that was fed in an amount equal to that consumed by a paired mate fed the (-)Zn diet, (+)ZnPF. Rats were killed after consuming their respective diets for 3, 5 and 7 weeks. Rats from (-)Zn had reduced body weight gain and testis weight at each wk sampled. They showed compromised zinc status as evidenced by reduced weight gain, and low serum and testis zinc concentrations. At each period, rats fed (-)Zn had significantly lower testicular ACE activity than rats fed either of the zinc adequate diets. Coinciding with the reduction in ACE activity at wk 5 and 7, but not at wk 3, there was a lower relative abundance of ACE mRNA in the (-)Zn group than in either of the zinc adequate groups. The results suggest that low ACE activity in the testis of rats in the early stages of zinc deficiency is caused by a reduction in mRNA translation, but in the latter stages of the deficiency, it is caused primarily by inhibition of ACE gene transcription.