The immunotoxic potential of glycidol was evaluated in female B6C3F1 mice u
sing a battery of functional assays and three host resistance models. Glyci
dol 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 ti
er I, we observed that glycidol exposure produced a dose-related decrease i
n splenocyte IgM antibody-forming cell response to sheep red blood cells (s
RBC); the spleen natural killer (NK) cell activity was also decreased. A de
crease in B cell proliferative responses to anti-IgM F(ab')(2) and/or inter
leukin-4 (IL-4) was observed while the splenocyte proliferative responses t
o T cell mitogen ConA and B cell mitogen LPS were not affected. The splenoc
yte proliferative response to allogeneic cells as evaluated in the mixed le
ukocyte 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 nu
mber of total T cells, CD8(+) T cells and CD4(+) CD8(+) T cells was not aff
ected. The cytotoxic T lymphocyte (CTL) response to mitomycin C-treated P81
5 mastocytoma was not affected; the cytotoxic activity of peritoneal macrop
hages was not suppressed. Moreover, the host resistance to Listeria monocyt
ogenes was not affected although a slight increase in host resistance to St
reptococcus pneumoniae was observed. However, exposure to glycidol decrease
d host resistance to the B16F10 melanoma tumor model with the maximal tumor
formation in lung observed in the high dose group. Overall, these dada sup
port the finding that glycidol is an immunosuppressive agent in female B6C3
F1 mice.