Di (2-ethylhexyl) phthalate facilitates the progression of alcoholic fatty liver via mediating oxidative stress injury and lipid peroxidation in rats

Abstract

Background: Long-term excessive drinking can cause various harms to the human body. Alcoholic fatty liver is the manifestation of early liver lesions mainly induced by alcohol. Di-(2-ethylhexyl) phthalate, as one of the environmental internal-secretion interfering-substance, is widely used in industrial processing and various consumer goods. Large quantities of epidemiological investigations and studies have shown that frequent exposure to high concentrations of DEHP may be a potential risk factor for liver function. Methods: We used DEHP to expose alcohol-induced fatty liver rats to study the effect of DEHP on alcoholic fatty liver. Results: The results found that DEHP exposure prominently accelerated hepatic steatosis, inflammation and oxidant stress, and activates signaling pathways involved in liver inflammation and oxidative stress-related proteins expression. Studies have suggested that cytochrome P450 2E1 and silent information regulator-1 are closely related to the occurrence of alcoholic fatty liver disease. Interestingly, the trend observed in the LO-2 cells assay was consistent with the in vivo conditions. Conclusions: DEHP may promote or aggravate the progression of alcoholic fatty liver disease through CYP2E1, SIRT1 and p38 mitogen-activated protein kinase (p38MAPK) / nuclear factor-kappa B signaling pathways. And this experimental study warns us that the environmental pollutants DEHP and its potential toxicity hazards to the human body are worthy of attention.