Gut microbiota dysbiosis might be responsible to different toxicity caused by Di-(2-ethylhexyl) phthalate exposure in murine rodents. (June 2020)

• Record Type: Journal Article
• Authors: Wang, Gang; Chen, Qian; Tian, Peijun; Wang, Linlin; Li, Xiu; Lee, Yuan-kun; Zhao, Jianxin; Zhang, Hao; Chen, Wei
• Is Part Of: Environmental pollution. Volume 261(2020)
• Publication Date: 2020-06
• Subjects: Di-(2-ethylhexyl) phthalate -- Murine rodents -- Toxicity -- Gut microbiota; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2020.114164
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: Di-(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer, which can enter the body through a variety of ways and exerted multiple harmful effects, including liver toxicity, reproductive toxicity and even glucose metabolism disorder. Many studies have suggested that changes of gut microbiota are closely related to the occurrence of various diseases, but the effects of DEHP exposure on gut microbiota are still unclear. It was found in this study that the damage to different tissues by DEHP on two strains each from two different species of male rodents before puberty was dose and time of exposure dependent, and also depending on the strain and species of rodent. Sprague-Dawley (SD) rats showed highest sensitivity to DEHP exposure, with most severe organ damage, highest Th1 inflammatory response and most significant body weight gain. Correspondingly, the gut microbiota of SD rats showed most significant changes after DEHP exposure. Only SD rats, but not Wistar rats, BALB/c and C57BL/6J mice showed an increase in Firmicutes/Bacteroidetes ratio and Proteobacteria abundance in the fecal samples, which are known to associate with obesity and diabetes. This is consistent with the increasing body weight gain which was only found in SD rats. In addition, the decrease in the level of butyrate, increase in the abundance of potential pathogens and microbial genes linked to colorectal cancer, Parkinson's disease, and type 2 diabetes in the SD rats were associated with issue and functional damages and Th1 inflammatory response caused by DEHP exposure. We postulate that the differential effects of DEHP on gut microbiota may be an important cause of the differences in the toxicity on different strains and species of rodents to DEHP. Graphical abstract: Image 1 Highlights: SD rats show most severe organ damage caused by DEHP in 4 strains of rodents. Only SD rats show significant body weight gain cause by DEHP exposure. SD rats show gut microbiota changes corresponding to weight gain and body damage. Gut microbiota dysbiosis may be the cause of the susceptibility of SD rats to DEHP. Abstract : Main finding: Among 2 strains each from 2 species of male murine rodents before puberty, SD rats showed highest sensitivity to DEHP exposure. The susceptibility of SD rats to DEHP exposure probably be related to the changes in gut microbiota.