||Comparative Immunosuppression of Various Glycol Ethers Orally Administered to Fisher 344 Rats.
Smialowicz, R. J. ;
Williams, W. C. ;
Riddle, M. M. ;
Andrews, D. L. ;
Luebke, R. W. ;
||Health Effects Research Lab., Research Triangle Park, NC. ;ManTech Environmental Technology, Inc., Research Triangle Park, NC.
Antibody formation ;
Alcohol dehydrogenase ;
Enzyme inhibitors ;
Ethylene glycol ;
Glycol ethers ;
||Some EPA libraries have a fiche copy filed under the call number shown.
||Oral dosing of adult male F344 rats with the glycol ether 2-methoxyethanol (ME) or its principal metabolite 2-methoxyacetic acid (MAA) results in the suppression of the primary plaque-forming cell (PFC) response to trinitrophenyl-lipopolysaccharide (TNP-LPS). In the present study, the PFC response to TNP-LPS was used to evaluate the immunotoxic potential of ethylene glycol (EG) as well as the glycol ethers 2-methoxyethyl acetate (MEA), 2-(2-methoxyethoxy) ethanol, bis(2-methoxyethyl) ether, 2-ethoxyethanol and its principal metabolite 2-ethoxyacetic acid, 2-ethoxyethyl acetate, and 2-butoxyethanol relative to ME and MAA. Rats were immunized with TNP-LPS and then exposed 4 and 28 hr later to 50, 100, 200, or 400 mg/kg of glycol ether or EG. Three days following immunization, the PFC response to TNP-LPS was determined. In addition to ME and MAA, only MEA, which was as effective as ME, suppressed the PFC response to TNP-LPS. Concomitant administration of the alcohol dehydrogenase inhibitor 4-methylpyrazole with ME or MEA prevented suppression of the PFC response by these glycol ethers. (Copyright (c) 1992 by the Society of Toxicology.)
||Pub. in Fundamental and Applied Toxicology 18, n4 p621-627 May 92. Prepared in cooperation with ManTech Environmental Technology, Inc., Research Triangle Park, NC.
|NTIS Title Notes
||Reprint: Comparative Immunosuppression of Various Glycol Ethers Orally Administered to Fisher 344 Rats.
||PC A02/MF A01