Macrophage tumoricidal mechanisms are selectively altered by prenatal chlordane exposure

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Abstract
Macrophages (mø) derived from mice treatedin utero with chlordane show a significant delay of tumoricidal induction activity. In this study, mø from chlordane-treated animals required a 48 hin vitro period of induction with interferon-ψ and lipopolysaccharide (IFN/LPS) before they could kill P815 targets. Similarly, mø from chlordane-treated animals also failed to produce an immediate H2O2 burst upon perturbation. Conversely, their stimulated control mø counterparts were tumoricidal by 2 h and exhibited a respiratory burst without any delay. Moreover, levels of the second messenger, inositol triphosphate (IP3), were significantly delayed in chlordane-treated animals following interaction with IFN/LPS. When nitrate/nitrite production was analyzed as an alternate mechanism for killing tumors, stimulated mø from both normal and chlordane-treated animals responded equally. The data show that chlordane differentially introduces defects in mø biochemical mechanisms associated with tumor killing.