The immunotoxic potential of
glycidol was evaluated in female B6C3F1 mice using a battery of functional assays and three host resistance models.
Glycidol was administered to the animals by oral gavage as a
solution in sterile distilled water daily for 14 days at doses of 25, 125 and 250 mg/kg. In tier I, we observed that
glycidol exposure produced a dose-related decrease in splenocyte
IgM antibody-forming cell response to sheep red blood cells (sRBC); the spleen natural killer (NK) cell activity was also decreased. A decrease in B cell proliferative responses to
anti-IgM F(ab')2 and/or
interleukin-4 (IL-4) was observed while the splenocyte proliferative responses to T cell
mitogen ConA and B cell
mitogen LPS were not affected. The splenocyte proliferative response to allogeneic cells as evaluated in the mixed leukocyte reaction (MLR) to DBA/2 spleen cells was not affected. In tier II, we found that exposure to
glycidol decreased the number and percentage of B cells and the absolute number of CD4+ T cells in the spleen while the number of total T cells, CD8+ T cells and CD4+CD8+ T cells was not affected. The cytotoxic T lymphocyte (CTL) response to
mitomycin C-treated P815
mastocytoma was not affected; the cytotoxic activity of peritoneal macrophages was not suppressed. Moreover, the host resistance to Listeria monocytogenes was not affected although a slight increase in host resistance to Streptococcus pneumoniae was observed. However, exposure to
glycidol decreased host resistance to the B16F10
melanoma tumor model with the maximal
tumor formation in lung observed in the high dose group. Overall, these dada support the finding that
glycidol is an
immunosuppressive agent in female B6C3F1 mice.