Knutson D W, Vredevoe D L, Aoki K R, Hays E J, Levy L
Immunology. 1980 May;40(1):17-26.
The ability of the reticuloendothelial system (RES) to bind and catabolize soluble stable heat aggregates of 125I-IgG (A-IgG) was studied in mice given oral cadmium. Cadmium caused a delay in the circulation clearance of A-IgG in intact animals. The defect was due to impaired liver uptake of A-IgG and correlated with increased liver cadmium. Subsequent catabolism of bound A-IgG by liver slices was not affected. The defect was specific in that clearance of aggregated human serum albumin and colloidal carbon was normal in cadmium mice; this suggests that cadmium may affect either Fc or complement receptors of Kupffer cells in liver.
在口服镉的小鼠中研究了网状内皮系统(RES)结合和分解125I-IgG可溶性稳定热聚集体(A-IgG)的能力。镉导致完整动物体内A-IgG的循环清除延迟。该缺陷是由于肝脏对A-IgG的摄取受损,且与肝脏镉含量增加相关。随后肝脏切片对结合的A-IgG的分解代谢未受影响。该缺陷具有特异性,因为镉处理的小鼠中聚集的人血清白蛋白和胶体碳的清除正常;这表明镉可能影响肝脏中库普弗细胞的Fc或补体受体。