Imunotoxicidade de edulcorantes alimentares: riscos versus beneficios

Abstract

The search for a healthier life has made using sweeteners to replace sugar. In general, sweeteners decrease the incidence of cavities, obesity, and associated diseases, such as diabetes and hyperlipidemia. However, there are several questions about the safety of these sweeteners. This work aims to analyze the cytotoxic, genotoxic, and mutagenic effects of sweeteners saccharin, Sucralose, fructose and Stevia rebaudiana Bertoni in concentrations like those used in human consumption using human lymphocyte culture. For that, the cell culture was prepared using blood from a healthy self-titled individual, collected by venipuncture and the cells of interest were separated with Histopaque® 1,077. An effect curve was performed to establish the concentrations to be used, where cell proliferation and cell viability were analyzed. Genotoxicological parameters were analyzed by comet test and chromosomal instability. The effects of sweeteners on lymphocyte subpopulations were also analyzed. Besides, the sweeteners were subjected to computational tests. Through the dose-effect curve, the defined concentrations were 1 μg / mL, 10 μg / mL and 50 μg / mL for each sweetener. In the cytotoxicity analyzes, he noticed that Sucralose and Steviol caused a decrease in the number of lymphocytes. Already with fructose and saccharin, this proliferation was not affected. In cell viability, no sweetener caused a reduction in the number of lymphocytes, however in the test with lymphocyte subpopulations, saccharin showed inhibition of TCD3 +, TCD8 + and T double population lymphocytes; Steviol showed inhibition of TCD4 + lymphocytes and double population and sweeteners Sucralose and fructose showed inhibition of TCD4 +, TCD8 + and T double population lymphocytes. In the comet test, all sweeteners evaluated caused DNA damage in at least one concentration tested. In the chromosomal instability test, only fructose did not generate changes. By the In Silico test, it was possible to propose that the main mechanism involved for DNA damage and changes is related to the modulation of gene expression, interfering with proteins related to DNA damage replication, maintenance, and repair.