Experiments were conducted to investigate the role of prostaglandins (PG) in zinc absorption and biological functions (food intake and weight gain, alkaline phosphatase activity, T-cell-mediated immune response) and the role of zinc in PG synthesis. PG levels were modified by either changing their precursors (essential fatty acids) concentration in the diet or administering an inhibitor of their synthesis, aspirin or indomethacin. Zinc level was modified by controlling the dietary concentration;Weanling rats were fed the assigned diets for one month after which they were anesthetized with either. Samples from blood, gut contents and mucosa, liver, lung, and tibia were collected for zinc, PG, and alkaline phosphatase measurements. In another experiment blood was collected for PG, zinc, and lymphocyte stimulation with T-cell mitogen assays;The zinc deficient rats were less active, and had decreased food intake, weight gain, organ weight, plasma and tibia zinc concentrations and blastogenic response of lymphocytes to T-cell mitogens. There was no difference in food intake, weight gain and organ weights of rats treated with aspirin, indomethacin, or high essential fatty acid diet (PUFA) from that of control rats. Indomethacin, aspirin, and PUFA did not significantly change zinc concentrations in any of the tissues measured. Indomethacin and aspirin slightly decreased, the PUFA increased zinc concentration in the mucosa. The decrease, however, did not reach statistical significance. Alkaline phosphatase activity was not altered by PG, indomethacin, aspirin, or PUFA. Indomethacin increased the blastogenic response of peripheral blood lymphocytes to T-cell mitogens. There was more than 50% inhibition of PG synthesis by indomethacin and aspirin. This inhibition of PG synthesis, however, did not affect the zinc status of the rats as measured by general appearance, food intake, weight gain, organ weight, zinc concentration in different organs, serum alkaline phosphatase activity, and cell mediated immune response to T-cell mitogens. Safflower oil did not affect either PG level or zinc status of the rats;In most organs studied and for most PG measured both zinc deficiency and food restriction decreased PG level to the same extent. Zinc deficiency seemed to be more effective in reducing PGE(,1), PGF(,2(alpha)), and PGI(,2) level in the gut contents than food restriction alone. Zinc deficiency increased metabolite of PGE(,2(alpha)) in serum and incubated lung homogenates, significantly. This rise in metabolite of PGF(,2(alpha)) was associated with a slight decrease in PGF(,2(alpha)) in serum and incubated lung homogenates;Conclusions reached were: (1) Inhibition of PG synthesis by more than 50% did not affect the zinc status of the rats. (2) Zinc might be involved in controlling tissue level of PG by changing their degradation rate. (3) In the gastrointestinal tract zinc deficiency might affect secretion of PG into the gut lumen. (4) Zinc and PG deficiencies have opposite effects on the cell mediated immune response.