POLYMORPHONUCLEAR PHAGOCYTOSIS AND KILLING IN WORKERS EXPOSED TO INORGANIC MERCURY

Citation
Rcr. Perlingeiro et Mls. Queiroz, POLYMORPHONUCLEAR PHAGOCYTOSIS AND KILLING IN WORKERS EXPOSED TO INORGANIC MERCURY, International journal of immunopharmacology, 16(12), 1994, pp. 1011-1017
Citations number
31
Categorie Soggetti
Immunology,"Pharmacology & Pharmacy
ISSN journal
01920561
Volume
16
Issue
12
Year of publication
1994
Pages
1011 - 1017
Database
ISI
SICI code
0192-0561(1994)16:12<1011:PPAKIW>2.0.ZU;2-Z
Abstract
The ability of neutrophils to phagocytose- and kill Candida species as well as the splenic phagocytic function were investigated in workers from a mercury-producing plant. In the neutrophil phagocytosis study, two species of Candida were used since in individuals with myeloperoxi dase deficiency neutrophils are unable to kill Candida albicans, while Candida pseudotropicalis can be effectively lysed. Phagocytosis of bo th antigens and splenic phagocytic function were normal in all the wor kers studied. However, following ingestion of the organisms there was considerable reduction in the ability of neutrophils from exposed work ers to kill both species of Candida, and this was not explained by a m ild impairment of phagocytosis. After improvement in the hygiene condi tions in the factory, a new evaluation was performed, 6 months later, in the same workers and urinary mercury concentrations were determined monthly in each worker. Despite a significant reduction in urinary me rcury concentrations, a greater impairment in the ability of neutrophi ls to kill C. albicans was observed. The killing of C. pseudotropicali s presented no further impairment when compared to the previous evalua tion. These results suggest that impairment of the lytic activity of n eutrophils from workers with urinary mercury concentrations within the safe level for exposed population is due, at least in part, to some i nterference with myeloperoxidase activity. In addition, the mercury-NA DPH complex, once formed, could limit the utilization of reduced pyrid ine nucleotides by NADPH-dependent enzymes such as NADPH oxidase, ther eby inhibiting the PMN respiratory burst.