Increased T-lymphocyte dependent antibody production in female SJL/J mice following exposure to commercial grade malathion.
The organophosphate pesticide, malathion, was evaluated for effects on immune function in female SJL/J mice. Commercial grade malathion was dissolved in corn oil and administered at doses of 0.018-180 mg/kg to mice via oral gavage on alternate days for 28 days. Exposure to malathion did not alter brain acetylcholinesterase activity, body weight gain, organ/body weight ratios or food and water consumption during the treatment period. Malathion enhanced the primary IgM antibody response to sheep red blood cells (SRBCs) by approximately 150% (P<0.02) at all doses tested when the response was expressed per 10(6) viable spleen cells and per spleen. B-lymphocyte blastogenesis induced by lipopolysaccharide (LPS, P=0.10) was not affected by malathion exposure. T-lymphocyte blastogenesis induced by concanavalin A (ConA, P=0.23) and phytohemagglutinin (PHA-P, P=0.24) also was unaffected by treatment with malathion. Malathion had no effect on splenic macrophage phagocytosis (P>0.11). These results indicate that repeated oral administration of commercial-grade malathion increased antibody production following immunization with a T-lymphocyte dependent antigen at doses as low as 0.018 mg/kg, which is below the human allowable daily intake (0.02 mg/kg). These changes occurred in the absence of B- or T-lymphocyte hyper responsiveness or alterations in macrophage phagocytosis. Immune system alterations at a sub-clinical level following exposure to a commercial formulation of malathion may have an important impact on human and animal health risk assessment. Therefore, further investigation into the mechanisms responsible for the increased antibody production is warranted.
Johnson
Victor J
VJ
Department of Verterinary Biomedical Sciences, Western College of Verterinary Medicine, University of Saskatchewan, 52 Campus Drive, Sask., S7N 5B4, Saskatoon, Canada.
Rosenberg
Alan M
AM
Lee
Kwang
K
Blakley
Barry R
BR
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000917:Antibody Formation / Q000187:drug effects; D001921:Brain / Q000201:enzymology; D002455:Cell Division / Q000187:drug effects; D005260:Female; D006462:Hemolytic Plaque Technique; D007111:Immunity, Cellular / Q000187:drug effects; D007075:Immunoglobulin M / Q000096:biosynthesis; D007306:Insecticides / Q000633:toxicity*; D008294:Malathion / Q000633:toxicity*; D051379:Mice; D008815:Mice, Inbred Strains; D008934:Mitogens / Q000494:pharmacology; D009929:Organ Size / Q000187:drug effects; D010587:Phagocytosis / Q000187:drug effects; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology*; D015430:Weight Gain / Q000187:drug effects
D007075:Immunoglobulin M; D007306:Insecticides; D008934:Mitogens; D000110:Acetylcholinesterase; D008294:Malathion