Lead toxicity via arachidonate signal transduction to growth responses in the splenic macrophage
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1Department of Microbiology and Immunology, Albany Medical College, Union University, New York 12208.
Abstract:
Lead chloride modulated the macrophage cell surface growth signal-transduced, lipid second messenger prostaglandin E2 (PGE2), concomitant with cell differentiation. In virgin macrophage, PGE2 was increased by lead in a dose-dependent manner, suggesting suppression of the immune function (inversely regulated by PGE2). Upon stimulation by bacterial endotoxin, lead-treated cells displayed decreased PGE2 with immune augmentation as tested by zymosan particle ingestion. These effects were simulated by a glutathione synthesis inhibitor around 10 microM lead, and by cycloheximide around 50 microM lead, suggesting a mechanism similar to viral infection.