Study of the adipogenic potential of the pesticides simazine and promethrin in cell culture
Pesticides, endocrine disruptors, adipogenesis
Brazil is one of the countries that consumes the most pesticides in the world. Exposure to these compounds can generate disorders in endocrine metabolism, known as endocrine disruptors. Recent studies point to evidence that exposure to these substances may be associated with obesity and other metabolic disorders. Previous and not yet published studies from the research group I am part of demonstrate that some pesticides can promote lipid accumulation in cell cultures of 3T3-L1 cells, including ametrine, a compound belonging to the triazine group. Considering the high consumption of pesticides in Brazil and few studies regarding their deregulatory effects, this present study aimed to study the adipogenic potential of two compounds, simazine and promethrin, belonging to the same group as ametrine. To evaluate the adipogenic potential of pesticides, a cell differentiation assay was performed on 3T3-L1 cells. In this assay, 3T3-L1 cells were treated for 14 days with vehicle (DMSO), rosiglitazone or increasing concentrations of pesticides that promoted lipid accumulation. Considering that pesticides promoted lipid accumulation, a transfection and luciferase reporter gene assay was performed to evaluate the transcriptional effects of the compounds on the PPARγ and RXRα nuclear receptors. For this, HeLa cells were co-transfected with plasmids containing DNA complementary to the receptor and plasmids with their responsive elements fused to the luciferase reporter gene and treated for 24 hours with vehicle (DMSO), known agonists of the receptors under study or increasing concentrations of the pesticide simazine. and promethrin, it was observed that the pesticides under study did not present an agonist effect on the receptors evaluated. Considering that both simazine and promethrin promoted lipid accumulation in 3T3-L1 cells, an assay was performed to evaluate whether this effect is dependent on PPARγ. To this end, a cell differentiation assay was performed on 3T3-L1 cells, treated for 14 days in the presence or absence of the specific PPARγ antagonist T0090709, vehicle (DMSO), rosiglitazone or increasing concentrations of the pesticides simazine and promethrin. In this assay, a significant reduction in lipid accumulation was observed in cells treated in the presence of the PPARγ antagonist T0090709 in both pesticides, which suggests that the lipid accumulation promoted by the pesticides simazine and promethrin are dependent on the PPARγ receptor. The results obtained in this study can help to better understand the effects of these compounds on human and animal health. As well as generating incentives for research into more efficient compounds with fewer negative effects. However, more studies are needed.