Untitled Item Proteomics study on the mechanism of arsenic hepatotoxicity and the protective mechanism of Dictyophora polysaccharide against arsenic hepatotoxicity

Arsenic is a highly toxic environmental toxicant and a known human carcinogen. Long-term exposure to arsenic can cause liver injury. Dictyophora polysaccharide (DIP) is a biologically active natural compound found in the edible plant Dictyostelium. In this study, Sprague-Dawley (SD) rat model of As toxicity was established using a feeding method, followed by DIP intervention in rats with As-induced liver injury. The molecular mechanism of arsenic toxicity to rat liver and the protective effect of DIP were investigated by proteomic studies. The results showed that 172, 328 and 191 differentially expressed proteins (DEPs) were identified between the arsenic-exposed rats versus control rats (As/Ctrl), DIP-intervened rats versus arsenic-exposed rats (DIP+As/As), and DIP-intervened rats versus control rats (DIP+As /Ctrl), respectively, respectively. Among them, the expression of 90 DEPs in the As/Ctrl group were reversed by DIP treatment. Arsenic exposure causes dysregulation of metabolic pathways, mitochondria, oxidative stress, and apoptosis-related proteins in rat liver. However, DIP treatment reversed or restored the expression levels of these proteins, thereby attenuating the liver injury induced by arsenic exposure in rats. The results provide a new insight into for mechanism of liver injury induced by arsenic exposure and the intervention of DIP in arsenic poisoning