Nutritional zinc increases platelet reactivity

After ingestion of 220 mg zinc sulfate, platelet aggregation was evaluated at various time intervals (i.e., T = 0, 1, and 3 hr) and the autologous plasma analyzed by atomic absorption analysis. The zinc levels increased maximally some 0.4 ± 0.2 μg/ml within 3 hr after ingestion, which tor the entire blood pool corresponds to only 5% of the ingested zinc. Aggregation responses of platelet rich plasma (PRP), instigated with suboptimal levels of thrombin (<0.2 U/ml), ADP (<2 μM), epinephrine (<2 μM), collagen (<2 μg/ml), or PAF (<50 ng/ml), show significant improvement to at least one aggregant. Mean ± SEM values for Δ% aggregation increase are as follows: thrombin, 51 ± 10%; epinephrine, 21 ± 6%; ADP, 31 ± 6%; collagen 23 ± 6%; and platelet aggregating factor (PAF), 56 ± 6%. For controls, the platelets from one individual with Glanzmann thrombasthenia as well as four undosed volunteers exhibited no significant changes in platelet responsiveness. Increased platelet responsiveness to agonists after zinc sulfate ingestion was observed in PRP from blood collected in either citrate or heparin. We demonstrate that within a relatively short time period, single bolus of nutritional zinc intake can significantly increase platelet reactivity. These findings show that nutritional zinc availability is relevant to hemostasis and may pertain to the viability of platelet concentrates in blood banks.