AI Summary & Key Takeaways
AI InsightIn conclusion, the present study shows that melatonin induced protective effects against diabetes-induced lens oxidative injury through up-regulation of the GSH and GPx values but down-regulation of oxidative stress.
📌 3 Key Takeaways
Abstract
Hyperglycemia plays a critical role in the development and progression of diabetic cataract oxidative injuries via the increased reactive oxygen species (ROS) production. Melatonin has been considered a potent strong antioxidant that detoxifies a variety of ROS in many metabolic diseases. The present study was conducted to explore whether melatonin administration protects against diabetic lens oxidative injuries through modulation of reduced glutathione (GSH) and glutathione peroxidase (GPx) systems in streptozotocin (STZ)-induced diabetic rats. Thirty two rats were equally divided into four groups as control, STZ, melatonin and STZ and melatonin. The third and fourth groups received intraperitoneal 10 mg/kg melatonin for 2 weeks. For induction of diabetes in the second and fourth groups, intraperitoneal STZ (45 mg/kg) was given. Lipid peroxidation (MDA), total oxidant status and intracellular ROS levels in the lens were increased in STZ group although they were decreased by melatonin treatment. GPx activity, GSH concentration and total antioxidant status (TAS) were lower in STZ group than in control. However, the GSH concentration, GPx activity and TAS levels were recovered by melatonin. TAS was also higher in melatonin group than in the STZ and melatonin groups. In conclusion, the present study shows that melatonin induced protective effects against diabetes-induced lens oxidative injury through up-regulation of the GSH and GPx values but down-regulation of oxidative stress.