title: Immunotoxicological assessment of methyl parathion in female B6C3F1 mice.
abstract: Methyl parathion is a widely used agricultural insecticide, and the recent unlicensed use of this compound in homes has led to the evacuation of approximately 1100 persons in Mississippi. Although the primary concern in such cases of acute exposure is neurotoxicity, a few organophosphorus compounds apparently have immunotoxic effects at dosages that do not produce neurotoxic symptoms. The purpose of the present study was to determine if this is the case for methyl parathion. Female B6C3F1 mice were exposed to methyl parathion by gavage, daily for 7, 14, 2 1, or 28 d (at 6 mg/kg/d). Exposure for 14-28 d produced significant, dose-responsive inhibition of acetylcholin-esterase (the target molecule for methyl parathion-induced neurotoxicity) in brain or plasma, indicating that the compound was active. The following immunological parameters were evaluated: white blood cell counts and differentials, spleen and thymus weight and cellularity, splenic natural killer cell activity, nitrite production by peritoneal macrophages following activation in vitro, antibody response to sheep erythrocytes in vitro and in vivo, the cytotoxic T lymphocyte response to allogeneic tumor cells, and resistance to Streptococcus agalactiae and B16F10 melanoma cells. Methylparathion at 1 or 3 mg/kg/d significantly increased splenic natural killer cell activity. Nitrite production by macrophages was increased in mice treated with 1, 3, or 6 mg/kg/d. The antibody response to sheep erythrocytes in vitro was significantly suppressed, but the humoral response to sheep erythrocytes in vivo was not affected. The cytotoxic T-lymphocyte response to allogeneic tumor cells was not significantly affected. Host resistance was not significantly decreased. Although it remains possible that immunological parameters not tested here may be affected by methyl parathion, the present results do not suggest substantial immunotoxic potential for this compound.
authors.affiliation: Department of Biological Sciences, Mississippi State University, Mississippi State, USA.
authors.forename: P L
authors.initials: PL
authors.lastname: Crittenden
authors.forename: R
authors.initials: R
authors.lastname: Carr
authors.forename: S B
authors.initials: SB
authors.lastname: Pruett
mesh_terms: D000110:Acetylcholinesterase / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D004305:Dose-Response Relationship, Drug; D005260:Female; D007107:Immune System / Q000187:drug effects*; D007306:Insecticides / Q000276:immunology* / Q000633:toxicity*; D007694:Killer Cells, Natural / Q000276:immunology; D008743:Methyl Parathion / Q000276:immunology* / Q000633:toxicity*; D051379:Mice; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
chemical_list: D007306:Insecticides; D008743:Methyl Parathion; D000110:Acetylcholinesterase