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Zinc Deficiency and Impaired Platelet Aggregation in Guinea Pigs^1,2,

Department of Biochemistry, University of Missouri, Columbia, MO 65211

Previous studies have shown that acute zinc deficiency results in impaired platelet aggregation in humans and rats as well as decreased sensitivity to such aggregating agents as ADP, arachidonate and collagen. This study was designed to evaluate the effect of zinc deficiency on platelet function and other pathology in the guinea pig. Guinea pigs of mixed sex were fed a purified diet based on soybean protein (1 ppm Zn) or a similar control diet (100 ppm Zn). In one trial weanling guinea pigs, weighing about 150 g, were fed the diets for 22 days. Those fed the basal diet failed to grow after 2 weeks, and food consumption decreased at this time although it did not become cyclic. They developed skin lesions; zinc concentrations were decreased in plasma, red cells and liver. There was no effect on the packed cell volume. Guinea pigs weighing 350 g and fed the basal diet for 18 days showed little or no effect on growth rate and food intake, but tissue zinc levels were decreased. Plasma zinc dropped significantly within 24 hours. Platelet aggregation in response to minimal levels of ADP and a prostaglandin endoperoxide analog (U-44069) was severely impaired. Aggregation in response to bovine thrombin (1 unit/ml) was significantly delayed, but the partial response in the presence of indomethacin was not affected by zinc deficiency. The results suggest that impaired platelet aggregation is a general sign of zinc deficiency in mammals and that the function of the physiological eicosanoids is impaired.

KEY WORDS: • zinc deficiency • guinea pigs • platelet aggregation • prostaglandin endoperoxide analog • thrombin • ADP

¹ Contribution of the Missouri Agricultural Experiment Station, Journal Series No. 9153. Supported in part by Public Health Service Grant HL11614.

² A preliminary report of this work was presented at the 66th Meeting of the Federation of American Societies of Experimental Biology, New Orleans, LA, April, 1982. Fed. Proc. 41: 282, 1982 (abs.).

³ Present address: Center for Biochemical and Biophysical Sciences and Medicine, Harvard Medical School, Boston, MA 02115.

⁴ To whom correspondence should be addressed.

Manuscript received 19 July 1982.