Resistencia a la insulina inducida por exposición a metamidofos: participación del estrés oxidativo.

Abstract

induction of oxidative stress is a mechanism through which OP induces IR. The objective of this work was to evaluate whether MET is capable to generate IR in HepG2 cells. In addition, we investigated the relationship between IR and oxidative stress using an antioxidant (specific for ROS). Cytotoxicity was assessed with MTT and Neutral Red assays, changes in the levels of reactive intracellular oxygen species (ROS), malonaldehyde (MDA), reduced glutathione (GSH) and genotoxic damage were evaluated as biomarkers of oxidative stress. While glycogen levels, lipid content and uptake/consumption/production of glucose, GLUT2 levels and the translocation of GLUT4 in HepG2 cells were evaluated as indicators of insulin resistance. The results showed that MET induced oxidative stress and insulin resistance in HepG2 cells. On the other hand, the use of antioxidants decreases oxidative stress and biomarkers of insulin resistance in the cellular model. These results suggest that MET is capable to induce insulin resistance through the induction of oxidative stress.