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Department of Biochemistry, University of Missouri, Columbia, MO 65211
The pathological signs of zinc and essential fatty acid deficiencies are highly analogous and aspirin, an inhibitor of prostaglandin synthesis, produces similar pathology when fed at toxic levels. To investigate the possibility that impaired prostaglandin biosynthesis is involved in the etiology of zinc deficiency pathology, the plasma concentrations of three prostaglandin metabolites were determined in zinc-deficient and control rats. Immature male rats were fed a purified diet low in zinc (<1 ppm) for 3 weeks. Ad libitum- and pair-fed controls consumed a similar diet supplemented with 100 ppm zinc. The zinc-deficient rats had low plasma zinc and their plasma concentrations of 13,14-dihydro-15-keto PGF2
and 13,14-dihydro-15-keto PGE2 were significantly higher than those of the pair-fed controls. Plasma 6-keto-PGF1
was not different between the zinc-deficient and pair-fed groups, but was significantly lower in deficient rats than in ad libitum-fed controls. The pair-fed controls had significantly lower plasma concentrations of all three metabolites than did the ad libitum-fed control group. The results suggest no impairment of prostaglandin production in zinc-deficient male rats.
KEY WORDS: male rat zinc deficiency prostaglandin metabolites pair-fed
1 A contribution of the Missouri Agricultural Experiment Station, Journal Series No. 8923. Supported in part by National Institutes of Health Grant HL11614.
2 Author to whom correspondence should be addressed.
Manuscript received 26 July 1982.