The effect of cadmium chloride on the immune response in mice.

B R Blakley
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Abstract

Six week old BDF1 female mice were exposed to cadmium chloride in the drinking water at concentrations ranging from 0 to 50 micrograms/mL cadmium for three weeks. The humoral immune response against sheep red blood cells which is T-lymphocyte and macrophage dependent, was suppressed in a dose dependent fashion with the maximum suppression of 28.2% observed in the highest exposure group (P less than 0.0001). Mitogen studies demonstrated that cadmium was a weak mitogen, producing a dose-dependent enhancement of blastogenesis (P = 0.026). T-lymphocyte responses which were induced by concanavalin A were not affected by cadmium exposure (P = 0.284). A dose-dependent enhancement of the B-lymphocyte activity was produced in the presence of cadmium when the lymphocytes were induced with Escherichia coli, lipopolysaccharide, a B-lymphocyte mitogen (P = 0.007). These results suggest that the immunosuppressive effects of cadmium associated with the humoral immune response are not due to an impairment of lymphocyte proliferation, an intermediate step involved in the generation of an immune response. The immunosuppressive effects were produced at relatively low cadmium exposures as indicated by the renal cadmium concentrations suggesting that the immune systems is very vulnerable to the toxic effects of cadmium.

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氯化镉对小鼠免疫反应的影响。
六周龄BDF1雌性小鼠连续三周暴露于浓度为0 ~ 50微克/毫升镉的饮用水中。对t淋巴细胞和巨噬细胞依赖的绵羊红细胞的体液免疫反应呈剂量依赖性抑制,最高暴露组最大抑制率为28.2% (P < 0.0001)。有丝分裂原研究表明,镉是一种弱有丝分裂原,对胚发生产生剂量依赖性增强(P = 0.026)。刀豆蛋白A诱导的t淋巴细胞反应不受镉暴露的影响(P = 0.284)。在镉存在的情况下,用大肠杆菌、脂多糖、b淋巴细胞有丝分裂原诱导淋巴细胞时,b淋巴细胞活性呈剂量依赖性增强(P = 0.007)。这些结果表明,与体液免疫反应相关的镉的免疫抑制作用不是由于淋巴细胞增殖的损害,而淋巴细胞增殖是免疫反应产生的中间步骤。免疫抑制作用是在相对较低的镉暴露下产生的,正如肾脏镉浓度所表明的那样,这表明免疫系统对镉的毒性作用非常脆弱。
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