title: Modulation of respiratory burst activity and mitogenic response of human peripheral blood mononuclear cells and murine splenocytes and peritoneal cells by malathion.
abstract: Previous studies showed that acute administration of noncholinergic doses of malathion in vivo elevated the humoral immune and mitogenic responses but did not alter the generation of the cytotoxic T lymphocyte (CTL) response to alloantigen of splenocytes from treated mice. However, in vitro exposure to malathion suppressed the generation of a CTL response. In this study, the effects of in vivo and in vitro (with and without an NADPH-regenerating liver enzyme system) exposure to malathion on the mitogenic responses of murine splenocytes or respiratory burst activity of peritoneal cells were examined. The effect of in vitro exposure to malathion on the ability of human peripheral blood mononuclear cells (PBMC) to perform these functions was also examined. In vivo exposure to malathion significantly elevated proliferative responses of murine splenocytes to mitogens. Cell separation and reconstitution studies indicated that adherent splenocytes from treated mice could elevate the proliferative responses of nonadherent splenocytes from control mice. Alternatively, in vitro exposure of murine splenocytes or human PBMC to malathion or malathion metabolized by a liver enzyme system suppressed or did not change, respectively, the proliferative responses to mitogens. In addition, cell separation and reconstitution experiments indicated that in vitro exposure to malathion affected nonadherent splenocytes and PBMC. In vivo exposure to malathion also elevated the production of hydrogen peroxide, following stimulation with phorbol myristate acetate, by murine peritoneal cells. In vivo exposure of murine peritoneal cells to malathion suppressed or elevated the respiratory burst activity following exposure to malathion or malathion metabolized by a liver enzyme system, respectively. Exposure of human PBMC to metabolized malathion in vitro enhanced their ability to produce hydrogen peroxide.
authors.affiliation: University of Southern California School of Medicine, Livingston Reproductive Biology Laboratory, Los Angeles 90033.
authors.forename: K E
authors.initials: KE
authors.lastname: Rodgers
authors.forename: D D
authors.initials: DD
authors.lastname: Ellefson
mesh_terms: D000818:Animals; D002469:Cell Separation; D005260:Female; D006861:Hydrogen Peroxide / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D008214:Lymphocytes / Q000187:drug effects; D008294:Malathion / Q000633:toxicity*; D051379:Mice; D008810:Mice, Inbred C57BL; D008934:Mitogens / Q000494:pharmacology*; D009000:Monocytes / Q000187:drug effects; D009249:NADP / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects*; D010529:Peritoneal Cavity / Q000166:cytology*; D013154:Spleen / Q000166:cytology / Q000187:drug effects*
chemical_list: D008934:Mitogens; D009249:NADP; D006861:Hydrogen Peroxide; D008294:Malathion