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COMPARATIVE IMMUNOSUPPRESSION OF VARIOUS GLYCOL ETHERS ORALLY ADMINISTERED TO FISCHER 344 RATS
Citation:
Smialowicz, R., W. Williams, M. Riddle, D. Andrews, R. Luebke, AND C. Copeland. COMPARATIVE IMMUNOSUPPRESSION OF VARIOUS GLYCOL ETHERS ORALLY ADMINISTERED TO FISCHER 344 RATS. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-92/230 (NTIS PB92195833), 1992.
Description:
Oral dosing of adult rats 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). n 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 (MEE), bis(2-methoxyethyl) ether (BMEE), 2-ethoxyethanol (EE) and its principal metabolite 2-ethoxyacetic acid (EAA), 2-ethoxyethyl acetate (EEA), and 2-butoxyethanol (BE) relative to ME and MAA. ats were immunized with TNP_LPS and then exposed 4 and 28 hours later to 50, 100, 200 or 400 mg/kg of each glycol ether or EG. hree days following immunization, the PFC response to TNP_LPS was determined. n addition to ME and MAA, only MEA, which was as effective as ME, suppressed the PFC response to TNP-LPS. oncomitant administration of the alcohol dehydrogenase inhibitor 4-methylpyrazole with ME or MEA prevented suppression of the PFC response by these glycol ethers. hese results indicate that of the chemicals tested only ME, MEA and MAA are immunosuppressive, and that oxidative metabolism via alcohol dehydrogenase is necessary for ME- and MEA-suppression of the response to TNP_LPS.