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Johnson KW, Holsapple MP, Munson AE: An immunotoxicological evaluation of gamma-chlordane. . Fundam Appl Toxicol. 1986 Feb;6(2):317-26.
Various toxicological and immunological parameters were assessed after exposure of female B6C3F1 mice to 0.1, 1.0, 4.0, and 8.0 mg/kg gamma-chlordane for 14 days via oral gavage. Variables evaluated included periodic body weights, terminal organ weights, hematology including leukocyte differentials, antibody response to sheep red blood cells (SRBC), lymphoproliferative responses to the mitogens phytohemagglutinin (PHA), concanavalin A (Con A), and lipopolysaccharide (LPS) and allogeneic cells, and the delayed hypersensitivity response (DHR) to keyhole limpet hemocyanin (KLH). When compared to the corn oil (vehicle) controls, chlordane produced a significant, dose-related increase in liver weight. Total leukocytes were significantly increased in chlordane-treated groups and seemed to be due to a significant increase in the lymphocyte population. Humoral immunity (HI), as assessed by enumeration of SRBC-specific immunoglobulin M (IgM) antibody forming cells (AFC) and proliferation of LPS-stimulated spleen cells, was not significantly altered in mice exposed to chlordane. In vitro evaluation of cell-mediated immunity (CMI), as measured by proliferation of Con A and PHA-stimulated spleen cells from chlordane-treated animals, indicated a significant and dose-related increase. The response to allogeneic cells was also enhanced. Results from an in vivo indicator of cell-mediated immune status, the delayed hypersensitivity response to KLH, did not support chlordane-enhanced T cell function suggested by mitogen and mixed lymphocyte responses. Therefore, a potent cyclodiene insecticide of environmental concern produced an enhancement of certain indicators of CMI. The expression of a DHR in vivo and the antibody response to SRBC was unaltered in mice exposed to the chemical. These results suggest that gamma-chlordane, at the concentrations utilized, does not produce a biologically significant alteration of the immunocompetence of intact animals. |
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