Dietary Se supplementation partially restores the REDOX proteomic map of M. spretus liver exposed to p,p'-DDE.

The toxicity of p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE), a contaminant and metabolite derivative of DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] is partially mediated by reactive oxygen species. Protein cysteine-based regulatory switches and subsequent alterations of the overall hepatic metabolism are triggered by p,p'-DDE through the disruption of the cellular redox status. The consequences are reproductive impairment, metabolic disorders, diabetes, neurotoxicity and cancer. In recent years, the risk of p,p'-DDE exposure has increased worldwide, reflecting the rise of mosquito-borne diseases in tropical countries that produce and export contaminated foods. Selenium (Se) is an essential trace element in animal nutrition with antioxidant properties that protects against the toxicity of some xenobiotics. We analyzed the ability of diet Se-supplementation to prevent damages induced by p,p'-DDE in the liver of M. spretus mice, by using redox proteomics based on the determination of the redox status of protein Cys residues. Se selectively acted on specific target, restoring the redox status and functionality of some membrane proteins involved in mitochondrial functionality, protein transport, cell signaling and protein metabolism. However, the Se-enriched diet did not completely prevent the metabolic shift caused by p,p'-DDE exposure that leads to disturbed lipogenesis, hepatic steatosis and alterations in the synthesis of hormones and other cell signals.