Many halogenated hydrocarbon pesticides are lipophilic and environmentally stable. Laboratory animal studies suggested that organo chlorine pesticides and related chemicals are tumorigenic. As these chemicals are not genotoxic their carcinogenic interactions are presumed to involve epigenetic effects. Our studies have focused on characterizing the epigenetic interactions of the halogenated hydrocarbons. We identified that in liver epithelial cells DDT, dieldrin and some polychlorinated biphenyl congeners inhibited intercellular communication mediated by gap junction proteins. The inhibition of gap junctional communication promotes clonal expansion of cancer initiated cells to become tumors. Investigations into the underlying mechanisms of tumor promoting interactions of DDT and dieldrin and PCB congeners revealed that exposure to these chemicals led to intracellular calcium surges from endoplasmic calcium pools to down regulate gap junction channel function as well as causing the activation of mitogenic signaling pathways mediated by the mitogen activated protein kinases (MAPKs) termed ERKS (extracellular signal regulated kinases).

Carcinogenic interactions of pesticides and related pollutants

248th National Meeting (2014)

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