Mercury intake by inflammatory phagocytes: in vivo cytology of mouse macrophages and neutrophils by X-ray elemental microanalysis coupled with scanning electron microscopy.

Phagocytes remove and store mercury (Hg) that enters the body. Macrophages and granulocytes respond in opposite ways to Hg: macrophages loose cell viability, and neutrophils become protected from apoptosis. We have investigated the cytology of early intake of Hg by macrophages and neutrophils after a short period (2-4 min) of in vivo exposure to HgCl2. The two types of phagocytes were attracted either to a subcutaneous air pouch or to the peritoneal cavity of BALB/c mice by in situ BSA injection. BSA caused, 72 hours later, inflammatory exudates where neutrophils (air-pouch cavity) or macrophages (peritoneal cavity) were the predominant cell type. A lethal dose of HgCl2 (25 mg) was then injected in the two inflammatory cavities. The mice died 2-4 min later and the cell exudates were harvested and studied by scanning electron microscopy coupled with X-ray elemental microanalysis (SEM-XRM). More than half of the phagocytes showed ingested Hg; a higher percentage of macrophages (around 70%) than neutrophils (around 50%) were positive for the metal. Intracellular particles of Hg were spheroid and presented a small diameter (less than 20 nm). They could be seen in large numbers inside phagocytes (up to 20-30 Hg dots per cell); they were scattered throughout the cytoplasm of the cells. The ability of phagocytes to ingest Hg increased as the BSA-induced inflammation progressed. We conclude that (i) Hg is quickly ingested as small particles by phagocytes; (ii) endocytosis of Hg increases with the degree of activation of phagocytes; and (iii) phagocytes internalize Hg by pinocytosis.