Inhalation of 1-bromopropane alters hippocampal expression of pathways related to immune system/inflammation and insulin signaling in experimental rats.

1-Bromopropane, an alternative to ozone-depleting solvents, exhibits neurotoxicity in humans and rats. The aim of the present study was to identify the genes or signaling pathways involved in the neurotoxicity and hepatotoxicity of 1-bomopropane in two inbred strains of rats. F344 rats and WNA/NUM rats were exposed to 1-bromopropane or filtered air by inhalation for either a single 8-hour session, or 8 h daily for 4 weeks. Motor nerve conduction velocity and distal latency were measured in the tail. At the end of the experiment, the animals were decapitated, and the hippocampus, liver, and blood were collected. Exposure to 1-bromopropane for 4 weeks increased distal latency in the tail nerve significantly in F344 and marginally in WNA/NUM. It also increased total and direct bilirubin in both rat strains. Eight-hour exposure increased metallothionein 2A, metallothionein 1 and NAD(P)H quinone dehydrogenase 1 expression in the liver of both rat strains, whereas 4-week exposure upregulated glutathione S-transferase alpha 3 and CD36 molecule in the liver of both strains. KEGG analysis showed that 8-hr 1-bromopropane upregulated pathways of apoptosis, NOD-like receptor signaling and colorectal cancer, in both the hippocampus and liver, whereas 4-week exposure upregulated NOD-like receptor signaling pathway both in the hippocampus and liver of the two rat strains. Insulin signaling pathway was upregulated persistently in the hippocampus of the two rat strains. Our results suggest the involvement of immune system/inflammation-related pathway in the neuro- and hepato-toxicity of 1-bromopropane and the involvement of insulin signaling pathway in the neurotoxicity of 1-brromopropane.