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Effect of mercuric chloride on microbicidal activities of human polymorphonuclear leukocytes
1Institute of Hygiene, University of Düsseldorf, F.R.G.
Abstract:
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.
Insights
Mercuric chloride impairs human polymorphonuclear leukocytes (PMNL) microbicidal functions, reducing phagocytosis and toxic oxygen species formation. However, it enhances lysozyme release, potentially impacting infection defense and causing inflammation.
Area of Science:
- Immunology
- Toxicology
- Cell Biology
Background:
- Human polymorphonuclear leukocytes (PMNL) are crucial for innate immunity.
- Mercuric chloride (HgCl2) is a known environmental toxicant.
- Understanding HgCl2 effects on immune cells is vital for public health.
Purpose of the Study:
- To investigate the impact of mercuric chloride on key human PMNL functions.
- To assess alterations in phagocytic capacity, reactive oxygen species (ROS) generation, and lysosomal enzyme release.
Main Methods:
- Human PMNL were exposed to varying concentrations of mercuric chloride.
- Phagocytic capacity was measured.
- Formation of toxic oxygen species was assessed using different activation methods (phagocytosis, Fc-receptor, PMA).
- Release of lysosomal enzymes (lysozyme, beta-glucuronidase) was quantified.
Main Results:
- Mercuric chloride significantly reduced PMNL phagocytic capacity in a dose-dependent manner.
- HgCl2 diminished toxic oxygen species formation, even when cells were activated without phagocytosis.
- Lysozyme release was enhanced by HgCl2, while beta-glucuronidase release remained unaffected.
- Cell viability was largely preserved at the tested concentrations.
Conclusions:
- Mercuric chloride compromises critical microbicidal functions of human PMNL.
- These alterations may lead to increased susceptibility to infections.
- Enhanced lysosomal enzyme release could contribute to inflammatory responses in surrounding tissues.