Modification of Oxidative Stress Induced by Exposure to Arsenate in Rat Chondrocytes Treated With Chitosan-Glutathione Nanoparticles.

Nanoparticles can modify the signaling pathways related to the toxic effects of xenobiotics and their toxicity by adding compounds that alter the oxidation-reduction state, such as glutathione (GSH). This work aimed to evaluate the antioxidant capacity of chitosan-glutathione nanoparticles (NPs Q-GSH) to modify lipoperoxidation induced by sodium arsenate using a primary culture of rat chondrocytes as a model. NPs Q-GSH were characterized in size (205.4 ± 33.35 nm), zeta potential (25.6 mV), and percentage of GSH (99.97%). To determine whether the toxicity of sodium arsenate was modified, chondrocytes were exposed to two concentrations of nanoparticles (0.08 and 0.64 μM GSH) for 2 h, followed by a 2-h acute exposure to sodium arsenate at a concentration of 1 × 10 M, and the determinations associated with the redox state were carried out. ANOVA was performed, followed by multiple analyses of Fisher's means with a p < 0.05. Regarding the measurement of biomarkers, an increase in GSH levels was observed, which can be both synthesized by the cell and provided by the NPs Q-GSH. A reduction in malondialdehyde levels was observed in the presence of an oxidizing agent, such as sodium arsenate, and subsequent exposure to NPs. Finally, the activity of the enzyme glutathione peroxidase increased significantly compared with untreated cells, which may be associated with GSH being its substrate and, therefore, favoring the activation of this enzyme. The activity of superoxide dismutase decreased, as did the levels of oxidized proteins. These systems could modify the signaling pathways associated with the redox state.