Truncated deoxynivalenol-induced splenic immediate early gene response in mice consuming (n-3) polyunsaturated fatty acids.

Expression profiling has previously revealed that acute exposure to the common foodborne mycotoxin deoxynivalenol (DON) induces a large number of immediate early genes in murine lymphoid tissues that potentially affect immune function. The purpose of this study was to test the hypothesis that consumption of (n-3) polyunsaturated fatty acids (PUFAs) found in fish oil interferes with DON-induced immediate early gene expression. Mice were fed AIN-93G diet containing 1% corn oil (CO) plus 6% oleic acid (control) or a diet containing 1% CO, 2% fish oil enriched in the (n-3)-PUFAs docosahexaenoic and eicosapentaenoic acid and 4% oleic acid.

Gene expression profiling in spleens of deoxynivalenol-exposed mice: immediate early genes as primary targets.

Exposure to the trichothecene mycotoxin deoxynivalenol (DON) alters immune functions in vitro and in vivo. To gain further insight into DON's immunotoxic effects, microarrays were used to determine how acute exposure to this mycotoxin modulates gene expression profiles in murine spleen. B6C3F1 mice were treated orally with 25mg/kg body weight DON, and 2h later spleens were collected for macroarray analysis.

Neutrophils contribute to endotoxin enhancement of allyl alcohol hepatotoxicity.

Nontoxic doses of endotoxin (lipopolysaccharide, LPS) enhance the hepatotoxicity of many xenobiotic agents, including allyl alcohol. Systemic LPS exposure induces an inflammatory response, including accumulation and activation of neutrophils (PMNs) in the liver. The hypothesis that PMNs play a causal role in LPS enhancement of allyl alcohol hepatotoxicity was tested.

Enhancement of allyl alcohol hepatotoxicity by endotoxin requires extrahepatic factors.

Noninjurious doses of bacterial endotoxin (lipopolysaccharide; LPS) enhance allyl alcohol-induced liver damage in rats in a Kupffer cell (KC)-dependent fashion. To investigate the mechanism by which KCs contribute to liver injury in this model, isolated KCs and hepatocytes (HCs) were cocultured. Addition of LPS to the cocultured cells did not enhance allyl alcohol-induced cytotoxicity.