Immune responses in rats supplemented with selenium.

It is generally accepted that Selenium (Se) is necessary for optimum performance of the immune system. Selenium deficiency results in immune suppression but little is known concerning the effect of excess Se on immune function. Recent evidence suggests that oral Se supplementation may impede oncogenesis, but the mechanism of this action is currently unknown. Conversely, under certain conditions, Se is suspected of promoting neoplasia. The studies described herein delineate the effects of excess Se (0.5, 2.0 or 5.0 p.p.m.) on specific immune functions of Se-adequate rats, namely, antibody synthesis, delayed-type hypersensitivity (DTH), natural killer (NK) cell activity, prostaglandin E2 (PGE2) synthesis, and interleukin 1 (IL-1) activity. Selenium administered to female Sprague-Dawley rats for 10 weeks at 0.5 and 2.0 p.p.m. resulted in significant (P less than or equal to 0.01) enhancement of splenic NK activity while the NK response in the 5.0 p.p.m. Se-treated rats was equivalent to the non-Se-treated controls. Conversely, the DTH response was significantly (P less than or equal to 0.01) suppressed at all three dosages while antibody synthesis and prostaglandin E2 activity were significantly (P less than or equal to 0.05) reduced compared to the controls at the highest dosage of Se. IL-1 activity was unaffected by Se exposure. These data could partially explain the contradictory oncogenic characteristics of Se. For instance, tumours that are NK sensitive could be prevented and/or responsive to Se therapy, while NK insensitive neoplasms could be enhanced by Se supplementation due to the impaired function of both humoral and cell-mediated immunity.