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慢性镉暴露后小鼠单核吞噬细胞系统的恢复

Recovery of the murine mononuclear phagocytic system following chronic exposure to cadmium.

作者信息

Vredevoe D, Levy L, Knutson D, Cook G, Cohen P

出版信息

Environ Res. 1985 Aug;37(2):373-82. doi: 10.1016/0013-9351(85)90118-5.

Abstract

Consistent with our previously reported findings, chronic ingestion of cadmium chloride in drinking water by mice caused a decrease in the rate of circulation clearance of 51Cr-labeled sheep red blood cells (E) and IgG-coated E (E-IgG) due to a decrease in the localization of E and E-IgG in the liver. These decreases reached their nadirs after 15 weeks of cadmium ingestion and remained relatively constant for up to one year during continued ingestion of cadmium. Replacement of the drinking water containing cadmium with regular tap water resulted within 8 days in an improvement in the ability of the mice to clear E and E-IgG. Mice also had a decreased ability to develop delayed-type hypersensitivity reactions while being given cadmium; this abnormality also returned toward normal after withdrawal of cadmium. The return of these two responses toward control levels occurred while there was still a large organ burden of cadmium that was not measurably different from that at cessation of cadmium ingestion.

摘要

与我们之前报道的结果一致,小鼠长期饮用含氯化镉的水会导致51Cr标记的绵羊红细胞(E)和IgG包被的E(E-IgG)的循环清除率下降,原因是E和E-IgG在肝脏中的定位减少。在摄入镉15周后,这些下降达到最低点,并且在持续摄入镉的长达一年时间里保持相对稳定。用普通自来水替代含镉饮用水后,8天内小鼠清除E和E-IgG的能力得到改善。在给予镉的同时,小鼠发生迟发型超敏反应的能力也降低;在停止给予镉后,这种异常也恢复正常。这两种反应恢复到对照水平的同时,镉的器官负荷仍然很大,与停止摄入镉时相比没有明显差异。

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