Dioxin effect in association or not with Methylmercury in adipogenic differentiation

• Grant number: 16/02385-5
• Support Opportunities: Scholarships in Brazil - Master
• Start date: August 01, 2016
• End date: March 31, 2017
• Field of knowledge: Biological Sciences - Pharmacology - Toxicology
• Principal Investigator: Camila Peres Buzalaf
• Grantee: Mariana Liessa Rovis Sanches
• Host Institution: Pró-Reitoria de Pesquisa e Pós-Graduação. Universidade do Sagrado Coração (USC). Bauru , SP, Brazil

Abstract

Methylmercury (MeHg) and dioxins, persistent toxic pollutants in the environment, are widely associated with several diseases to human health and may cause cytotoxic effects with impact on the pathophysiology of nervous system, immune, cardiovascular, endocrine and developing genetic and carcinogenic diseases . Several studies have shown an association between exposure to these elements and the development of metabolic syndrome, a group of diseases associated with obesity such as diabetes type II.Insulin resistance characteristic of the type II diabetes is associated with altered metabolism of the adipocytes, cells differentiated from mesenchymal stem cells. Thus, understanding the mechanisms involved in cellular differentiation of adipose tissue may explain the development of diseases such as diabetes, associated or not with exposure to contaminants. Accordingly, literature shows that there is an inverse association between insulin resistance and adipogenic differentiation and the correlation between exposure and MeHg dioxins and the development of diabetes. However, little is known about the impact of these toxicants in doses that mimic those caused by poisoning in humans, and the potential antagonistic effects, and synergistic or additive in adipogenic differentiation from mesenchymal stem cells. The objective of this project is to evaluate qualitatively and quantitatively the effect of in vitro exposure to MeHg and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on adipogenic differentiation, through the deposition of triglycerides and by flow cytometry, respectively. Furthermore, the molecular mechanisms involved in the toxicity of these substances will be evaluated by proteomic analysis of different experimental conditions. Thus, it is intended to identify if there is this correlation and if yes, proteins that may be targets of toxicity caused by these contaminants found in the environment, which the human population is exposed. (AU)