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Mercury is a widespread metal and consequently there are large populations that currently exposed to low levels of mercury. Endotoxin is a component of the gram- negative bacte ria and promotes inflammatory responses. The present study was designed to determine the impact of mercury on lymphocytes phenotype populations and endotoxin- induced inflammatory cytokine expressions in immune organ, spleen and thymus. Male BALB/C mice were exposed continuously to 0, 0.3, 1.5, 7.5, or 37.5 ppm of mercuric chloride in drinking water for 14 days and at the end of the treatment period, lipopolysaccharide (LPS, 0.5 mg/kg) was injected intraperitoneally 2 h prior to euthanasia. The dose-range of mercury used did not cause hepatotoxicity, Mercury at 7.5 and 37.5 ppm dose-dependently decreased CD3+ T lymphocytes in spleen; both CD4+ and CD8+ single positive lymphocyte populations were decreased. Exposure to 7.5 and 37.5 ppm of mercury decreased the CD8+ T lymphocyte population in the thymus, whereas double positive CD4+/CD8+ and CD4+ thymocytes were not altered. Mercury altered LPS-induced inflammatory cytokine gene expressions such as, tumor necrosis factor α, interferon γ, and interleukin-12 in spleen and thymus. Results indicated that decreases in T lymphocyte populations in immune organs and altered frtokine gene expression may contribute to the immune-modulative effects of inorganic mercury.
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