Microplastics release phthalate esters and cause aggravated adverse effects in the mouse gut

Abstract

Increasing evidence shows that microplastics (MPs) have the potential to act as carriers and transport contaminants into organisms, as well as induce serious health risks. Here we endeavored to address for the first time whether MPs could transport and release phthalate esters (PAEs) into mouse gut and the consequential toxic effects. As a result, MPs could adsorb PAEs, transport PAEs into the gut and cause intestinal accumulation. The accumulation of PAE in the gut followed the order of DEHP > DBP > DEP > DMP, which was the same order for the adsorption of PAEs on MPs. After exposed to DEHP-contaminated MPs for 30 days, significantly increased intestinal permeability and enhanced intestinal inflammation were induced compared with individual MPs and DEHP according to biochemical and histological analysis. Transcriptomic analysis found that 703 genes were differentially regulated and these genes are involved in oxidative stress, immune response, lipid metabolism, and hormone metabolism. Moreover, gut microbiota analysis found that the combined exposure of MPs and DEHP also caused alterations in gut microbiota composition, especially some energy metabolism and immune function related bacteria were significantly changed in the relative abundance. The aggravated effects on intestinal inflammation and metabolic disorders caused by DEHP-contaminated MPs may attribute to increased DEHP accumulation, changed exposure pathway, and shared toxic mechanisms. Our results provide valuable information for the health risk of MPs and plastic additives.

Keywords: Gut; Joint toxicity; Microplastics; Mouse; Phthalate esters.