Krzystyniak K, Trottier B, Jolicoeur P, Fournier M
Département des Sciences Biologiques, Université du Québec à Montréal, Canada.
Mol Toxicol. 1987 Apr-Sep;1(2-3):247-59.
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.
在近交系C57Bl/6小鼠中,研究了某些有机氯、有机磷和氨基甲酸酯类农药对腹膜巨噬细胞功能和细胞参数的毒性。通过分析细胞活力、细胞黏附能力、超氧阴离子(O2-)的产生、抗原加工、鼠伤寒沙门氏菌的吞噬作用以及感染小鼠肝炎病毒3(MHV3)后对体外病毒诱导的细胞病变效应(CPE)的抵抗力,确定了单次亚致死剂量农药暴露对巨噬细胞的影响。大多数研究针对有机氯农药狄氏剂进行,它抑制了几种巨噬细胞功能,如鼠伤寒沙门氏菌的吞噬作用、单一加工蛋白抗原抗生物素蛋白的释放以及对MHV3病毒诱导的CPE的抵抗力。在体内暴露于单次亚致死剂量的其他选定农药(如谷硫磷、克百威、西维因和灭草灵)后,巨噬细胞培养物中病毒诱导的细胞溶解显著增加。然而,以亚致死剂量(0.4≤LD50≤0.6)使用的选定农药似乎都不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。总之,亚致死剂量的农药暴露可导致几种巨噬细胞功能显著受损,如吞噬作用、抗原加工以及对病毒诱导的细胞溶解的抵抗力。然而,亚致死剂量农药暴露抑制O2-生成系统可被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潜在抑制作用的机制。