Chlorpyrifos induces pro‐inflammatory environment in discrete regions of mouse brain

Abstract

It has been proposed that exposure to environmental toxicants plays a role in the development of neurodegenerative diseases. Mechanisms of action underlying this process, however, have not yet been clearly established. The present study was designed to address potential mechanisms that contribute to brain injury after exposure to the organophosphorus insecticide chlorpyrifos. C57BL/6 mice were administered a single intraperitoneal injection of chlorpyrifos in increasing dosages (20, 70, and 140 mg/kg). At 4, 8, 16, and 24 h of exposure, four discrete regions of the brain (hippocampus, cerebral cortex, striatum, and cerebellum) were isolated, and expression levels of pro-inflammatory mediators were assessed by quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR). A significant increase in expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), MCP-1, and E-selectin was observed in all brain regions in a time- and dose-dependent manner. These data suggest that chlorpyrifos-induced brain injury may be mediated through pro-inflammatory pathways. It also offers the potential to contribute to the development of new therapeutic strategies specifically targeted against pro-inflammatory pathways of environmental agent-induced neurotoxicity (This work was supported by SBES Seed Grants).