Baginski B
Institute of Hygiene, University of Düsseldorf, F.R.G.
Toxicology. 1988 Aug;50(3):247-56. doi: 10.1016/0300-483x(88)90042-x.
We investigated the effects of mercuric chloride on phagocytic capacity, formation of toxic oxygen species and release of lysosomal enzymes of human polymorphonuclear leukocytes (PMNL). Our results show that HgCl2 may alter these microbicidal functions of human PMNL without remarkable damage of cell viability. The phagocytic capacity was markedly depressed in a concentration-dependent manner. The formation of toxic oxygen species was also diminished by mercuric chloride when induced by phagocytosis. It was furthermore reduced when the PMNL were activated without phagocytosis by binding of IgG to Fc-receptors or by binding of phorbol myristate acetate to the membrane. In contrast, the release of the lysosomal enzyme lysozyme was enhanced in the presence of mercuric chloride, but not the release of beta-glucuronidase. These effects may lead to impaired defense against infections and possibly to inflammatory reactions in adjacent tissues induced by released lysosomal enzymes.
我们研究了氯化汞对人多形核白细胞(PMNL)吞噬能力、毒性氧物种形成及溶酶体酶释放的影响。我们的结果表明,HgCl2可能改变人PMNL的这些杀菌功能,而对细胞活力无明显损害。吞噬能力以浓度依赖的方式显著降低。当通过吞噬作用诱导时,氯化汞也会减少毒性氧物种的形成。当PMNL通过IgG与Fc受体结合或佛波酯肉豆蔻酸酯与膜结合在无吞噬作用的情况下被激活时,毒性氧物种的形成进一步减少。相比之下,在氯化汞存在的情况下,溶酶体酶溶菌酶的释放增强,但β-葡萄糖醛酸酶的释放未增强。这些影响可能导致抗感染防御受损,并可能导致由释放的溶酶体酶诱导的相邻组织的炎症反应。