Protective Roles of Selenium on Nitric Oxide and the Gene Expression of Inflammatory Cytokines Induced by Cadmium in Chicken Splenic Lymphocytes.

Abstract

Cadmium (Cd) is an environmental toxicant and an inflammation-related xenobiotic. Selenium (Se) is a well-known nutritional trace element and a potent chemopreventive agent. The present study aimed to investigate the effect of Se on the cytotoxicity of Cd in bird immunocytes in vitro. Chicken splenic lymphocytes exposed to CdCl2 (10(-6)mol/L), Na2SeO3 (10(-7)mol/L), or a mixture of the two (10(-7)mol/L Na2SeO3 and 10(-6)mol/L CdCI2) were incubated for 12, 24, 36, 48, or 60h. Cd significantly increased (P < 0.05 or P < 0.01) the messenger RNA (mRNA) expression levels of nuclear factor kappaB (NF-κB), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor (TNF-α), and prostaglandin E2 (PGE2), and similar results were observed in the protein expression levels of NF-κB and COX-2. In addition, the nitric oxide (NO) content and the inducible iNOS activity were increased in the Cd-treated group compared to the control group. Furthermore, the protective effects of Se against Cd toxicity in chicken splenic lymphocytes were illustrated by the increase in select cytokines (NF-κB, iNOS, COX-2, TNF-α, and PGE2), NO content and iNOS activity. The biochemical parameters exhibited sensitivity to Se and Cd, suggesting that they may act as potential biomarkers for assessing the effects of Se and Cd risk on chicken splenic lymphocytes.