the ameliorative effect of naringenin on paraquat-induced toxicity in mitochondria isolated from rats

results the results reveal that pq can decrease mitochondrial viability, deplete gsh content, increase mitochondrial ros formation, and enhance lpo and mitochondrial membrane damage. the pretreatment of mitochondria with ng has the ability to reduce the toxic effects of pq in isolated mitochondria. background paraquat (pq) is a dipyridyl herbicide that sustains damage due to redox cycling. an important aspect of pq toxicity is defined by its interactions with mitochondria. objectives this study was designed to evaluate the ability of naringenin (ng) to prevent pq-induced mitochondrial dysfunction in rat-isolated liver mitochondria. materials and methods to determine the ic50 of pq, the mitochondrial viability was specified using an mtt assay. different concentrations of pq (0, 2.5, 5, and 10 mm) were used, and the ic50 of pq was assigned as approximately 2 mm. the suspensions of mitochondria at concentrations of 0.5 mg protein/ml were exposed to different concentrations of ng (100, 200, and 400 µm) for 30 minutes and were then treated with pq at a concentration of ic50 (2 mm) for another 30 minutes at 37°c. the ameliorative effects of ng on pq toxicity were evaluated by determining the glutathione (gsh) content, the damage to the mitochondrial membrane, the reactive oxygen species (ros), and lipid peroxidation (lpo). conclusions the results suggest that the toxic effects of pq that are mediated through ng and mitochondria can be reversed in a concentration-dependent manner. in addition, ng may prevent the oxidative stress induced by pq. these results suggest that the administration of antioxidants such as ng may either restore the mitochondrial antioxidant status or improve mitochondrial functions, thus protecting mitochondria from oxidative damage.