Glycidol modulation of the immune responses in female B6C3F1 mice

被引:25
作者
Guo, TL
McCay, JA
Brown, RD
Musgrove, DL
Butterworth, L
Munson, AE
Germolec, DR
White, KL
机构
[1] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA
[2] NIEHS, Res Triangle Pk, NC 27709 USA
关键词
D O I
10.1081/DCT-100100127
中图分类号
O6 [化学];
学科分类号
0703 [化学];
摘要
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.
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收藏
页码:433 / 457
页数:25
相关论文
共 33 条
[1]
Abbas A.K., 1991, CELL MOL IMMUNOL, V1, P243
[2]
COMPARATIVE MUTAGENICITY OF ALIPHATIC EPOXIDES IN SALMONELLA [J].
CANTER, DA ;
ZEIGER, E ;
HAWORTH, S ;
LAWLOR, T ;
MORTELMANS, K ;
SPECK, W .
MUTATION RESEARCH, 1986, 172 (02) :105-138
[3]
THE LYMPHOCYTE-B IS THE IMMUNE CELL TARGET FOR 2',3'-DIDEOXYADENOSINE [J].
CAO, W ;
SIKORSKI, EE ;
FUCHS, BA ;
STERN, ML ;
LUSTER, MI ;
MUNSON, AE .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1990, 105 (03) :492-502
[4]
Fidler I J, 1978, Adv Cancer Res, V28, P149, DOI 10.1016/S0065-230X(08)60648-X
[5]
CHEMICAL MUTAGENESIS TESTING IN DROSOPHILA .10. RESULTS OF 70 CODED CHEMICALS TESTED FOR THE NATIONAL-TOXICOLOGY-PROGRAM [J].
FOUREMAN, P ;
MASON, JM ;
VALENCIA, R ;
ZIMMERING, S .
ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, 1994, 23 (03) :208-227
[6]
GEISSLER K, 1989, CANCER RES, V49, P3057
[7]
GERMOLEC DR, 1988, CANCER IMMUNOL IMMUN, V27, P121
[8]
HANNA N, 1981, J IMMUNOL, V127, P1754
[9]
Regulation of a S(trans-1,2-dichlorovinyl)-L-cysteine-Induced Renal Tubular Toxicity by Glutathione? [J].
Hassall, C. D. ;
Brendel, K. ;
Gandolfi, A. J. .
JOURNAL OF APPLIED TOXICOLOGY, 1983, 3 (06) :321-325
[10]
HOLSAPPLE MP, 1983, J PHARMACOL EXP THER, V227, P130