亚致死农药暴露后小鼠巨噬细胞功能活性与细胞参数的关系。

Molecular toxicology Pub Date : 1987-04-01
K Krzystyniak, B Trottier, P Jolicoeur, M Fournier
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引用次数: 0

摘要

研究了有机氯、有机磷和氨基甲酸酯农药对C57Bl/6小鼠腹腔巨噬细胞功能和细胞参数的毒性。通过分析小鼠肝炎病毒3型(MHV3)感染后巨噬细胞的细胞活力、细胞粘附能力、超氧阴离子(O2-)的产生、抗原加工、鼠伤寒沙门菌的吞噬和对体外病毒诱导的细胞病变效应(cpe)的抗性,确定单次、亚致死农药暴露对巨噬细胞的影响。大多数研究是针对有机氯农药狄氏剂进行的,狄氏剂抑制了巨噬细胞的几种功能,如鼠伤寒沙门氏菌的吞噬作用、单加工蛋白抗原亲和素的释放以及对MHV3病毒诱导的cpe的抗性。体内暴露于单次亚致死剂量的其他选定杀虫剂(如古硫磷、呋喃、七维安和马他西尔)后,巨噬细胞培养物中病毒诱导的细胞溶解显著增加。然而,在亚致死(0.4小于或等于LD50小于或等于0.6)剂量下使用的选定杀虫剂中,没有一种似乎是损害化学诱导或免疫激活的腹膜巨噬细胞中O2-生成系统的因素。综上所述,亚致死农药暴露可导致巨噬细胞的多种功能显著受损,如吞噬、抗原处理和对病毒诱导的细胞溶解的抗性。然而,亚致死农药暴露对O2-生成系统的抑制可以排除为这些农药对巨噬细胞起主要作用的抗病毒和抗菌宿主防御系统的潜在抑制作用的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Macrophage functional activities versus cellular parameters upon sublethal pesticide exposure in mice.

The toxicity of selected organochlorine, organophosphate, and carbamate pesticides on the functions and cellular parameters of peritoneal macrophages was examined in inbred C57Bl/6 mice. Effects of single, sublethal pesticide exposure on macrophages were determined by analysis of the cell viability, cell adherence capacity, generation of superoxide anion (O2-), antigen processing, phagocytosis of Salmonella typhimurium, and resistance to in vitro virus-induced cytopathic effects (cpe) after infection with mouse hepatitis virus 3 (MHV3). Most of the studies were done for the organochlorine pesticide dieldrin, which inhibited several macrophage functions, such as phagocytosis of S. typhimurium, release of the single processed protein antigen avidin, and resistance to MHV3 virus-induced cpe. The virus-induced cytolysis in macrophage cultures was significantly increased after in vivo exposure to single sublethal doses of other selected pesticides, such as guthion, carbofuran, sevin, and matacil. However, none of the selected pesticides, used in sublethal (0.4 less than or equal to LD50 less than or equal to 0.6) doses appeared to be a factor impairing the O2- -generating system in chemically elicited or immunologically activated peritoneal macrophages. In conclusion, sublethal pesticide exposure can induce a significant impairement of several macrophage functions, such as phagocytosis, antigen processing, and resistance to virus-induced cytolysis. Inhibition of the O2- -generating system by sublethal pesticide exposure, however, can be excluded as a mechanism of potential suppressory action of these pesticides on antiviral and antibacterial host defence systems in which macrophages play a primary role.

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