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Title: Perinatal immunotoxicity of benzene toward mouse B cell development

Abstract

Benzene is widely used by chemical industries and exposure to benzene has been shown experimentally to be immunotoxic in adult animals. The present study addressed whether exposure of fetuses in utero to benzene compromises the development of fetal B lymphopoiesis and whether B-lymphocyte development recovers postnatally. Pregnant BALB/C dams were given intraperitoneal injections of benzene (100 mg/kg, twice daily) from day 12.5 of gestation through day 19.5 of gestation. Phenotypic analysis revealed that fetal liver cell suspensions from embryos exposed in utero contained fewer pre-B cells and B cells than corresponding controls. Fetal liver cell cultures established from these embryos also produced fewer B cells. In contrast, pre-B cells were elevated in the livers of 8-day-old neonates that had been exposed to benzene in utero. Moreover, responsiveness to the B-cell mitogen, LPS, was significantly decreased in spleen cell cultures derived from these neonates. The results indicate that in utero exposure to high concentrations of benzene alters fetal B lymphopoiesis and may compromise immune responsiveness postnatally.

Authors:
; ; ; ;
Publication Date:
Research Org.:
West Virginia Univ., Morgantown, WV (USA)
OSTI Identifier:
7190064
Report Number(s):
PB-90-199407/XAB
Resource Type:
Technical Report
Resource Relation:
Other Information: Pub. in Jnl of the American College of Toxicology, Vol. 8, No. 5(1989)
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; BENZENE; TOXICITY; LYMPHOCYTES; CELL PROLIFERATION; BONE MARROW; CELL CULTURES; EMBRYOS; FETUSES; FLUORESCENCE; LIPOPOLYSACCHARIDES; LIVER; MICE; PHENOTYPE; PREGNANCY; SPLEEN; TERATOGENESIS; ANIMAL CELLS; ANIMAL TISSUES; ANIMALS; AROMATICS; BIOLOGICAL MATERIALS; BLOOD; BLOOD CELLS; BODY; BODY FLUIDS; CARBOHYDRATES; CONNECTIVE TISSUE CELLS; DIGESTIVE SYSTEM; GLANDS; HEMATOPOIETIC SYSTEM; HYDROCARBONS; LEUKOCYTES; LIPIDS; LUMINESCENCE; MAMMALS; MATERIALS; ORGANIC COMPOUNDS; ORGANS; POLYSACCHARIDES; RODENTS; SACCHARIDES; SOMATIC CELLS; TISSUES; VERTEBRATES; 560300* - Chemicals Metabolism & Toxicology

Citation Formats

Wierda, D, King, A, Luebke, R, Reasor, M, and Smialowicz, R J. Perinatal immunotoxicity of benzene toward mouse B cell development. United States: N. p., 1989. Web.
Wierda, D, King, A, Luebke, R, Reasor, M, & Smialowicz, R J. Perinatal immunotoxicity of benzene toward mouse B cell development. United States.
Wierda, D, King, A, Luebke, R, Reasor, M, and Smialowicz, R J. 1989. "Perinatal immunotoxicity of benzene toward mouse B cell development". United States.
@article{osti_7190064,
title = {Perinatal immunotoxicity of benzene toward mouse B cell development},
author = {Wierda, D and King, A and Luebke, R and Reasor, M and Smialowicz, R J},
abstractNote = {Benzene is widely used by chemical industries and exposure to benzene has been shown experimentally to be immunotoxic in adult animals. The present study addressed whether exposure of fetuses in utero to benzene compromises the development of fetal B lymphopoiesis and whether B-lymphocyte development recovers postnatally. Pregnant BALB/C dams were given intraperitoneal injections of benzene (100 mg/kg, twice daily) from day 12.5 of gestation through day 19.5 of gestation. Phenotypic analysis revealed that fetal liver cell suspensions from embryos exposed in utero contained fewer pre-B cells and B cells than corresponding controls. Fetal liver cell cultures established from these embryos also produced fewer B cells. In contrast, pre-B cells were elevated in the livers of 8-day-old neonates that had been exposed to benzene in utero. Moreover, responsiveness to the B-cell mitogen, LPS, was significantly decreased in spleen cell cultures derived from these neonates. The results indicate that in utero exposure to high concentrations of benzene alters fetal B lymphopoiesis and may compromise immune responsiveness postnatally.},
doi = {},
url = {https://www.osti.gov/biblio/7190064}, journal = {},
number = ,
volume = ,
place = {United States},
year = {Sun Jan 01 00:00:00 EST 1989},
month = {Sun Jan 01 00:00:00 EST 1989}
}

Technical Report:
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