镉免疫毒性的β-肾上腺素能受体机制研究

目的 探讨β－肾上腺素能受体（β受体）途径在镉（Ｃｄ）免疫毒性机制中的地位和作用。方法 运用β受体阻断剂心得安（Ｐｒｏ）建立肾上腺素能受体阻断的动物模型,观察镉韵及用心得安预处理阻断β肾上腺素能受体后其对脾淋巴细胞β受体密度、ｃＡＭＰ含量、ＤＮＡ损伤程度、Ｔ淋巴细胞增殖功能及Ｔ淋巴细胞亚群的影响。结果 当单独染镉时,脾淋巴细胞β－受体密度在中及高剂量染镉组高于对照组;脾淋巴细胞ｃＡＭＰ含量随镉浓度

Study on beta-adrenoceptors mechanism of cadmium immunotoxicity

OBJECTIVE: To study if the beta-adrenoceptors mechanism plays important role in the immunotoxicity of cadmium. METHODS: The beta-adrenoceptor density, cellular cyclic adenosine 3',5' monophosphate (cAMP) levels, and DNA damage of rat spleen lymphocytes were studied. Beta-antagonist propranolol was used to block the beta-adrenoceptor. RESULTS: In the single Cd administration group: beta-adrenoceptor density of spleen lymphocytes in the middle and high Cd concentration groups was higher than that in the non-Cd treated control group (P < 0.05), the levels of cAMP increased with the increase of Cd doses, and the result of the high Cd group was higher than that of the control group (P < 0.05). The proliferation function of T lymphocytes was lower in each Cd group than that in the control group (P < 0.05). Single cell gel electrophoresis (SCGE) detected that DNA damage of spleen lymphocytes in each Cd group were more severe than the control (P < 0.05). Pretreated with Pro group: After blocked with propranolol, beta-adrenoceptor density increased in the Pro control group and the density in all Cd treated groups was higher than the control group (P < 0.05), but all Cd treated groups showed no statistical significance than the Pro control group (P > 0.05). The cAMP levels, MTT and the subsets of T lymphocytes showed no statistical significance among all the groups (P > 0.05). The results of SCGE showed that DNA damage was most severe only in the high Cd group than other groups (P < 0.05). CONCLUSION: The results suggest that the nerve-internal secretion system plays an important role in the immunotoxicity of cadmium, and the beta-adrenoceptor mechanism is important in the immunotoxic mechanism of cadmium.