Diabetes-induced hyperglycemia disrupts the redox balance, leading to oxidative stress in the retina. Under normal physiological conditions, there is a balance in the production of reactive oxygen species (ROS)/reactive nitrogen species (RNS) and the antioxidant defense system. Diabetes-induced hyperglycemia promotes ROS/RNS generation while also suppressing the retinal antioxidant response, creating the imbalance known as oxidative stress. The AGE pathway, the polyol pathway, the hexosamine biosynthetic pathway (HBP), and the protein kinase C pathway are all sensitive to this disruption and play an important role in the downstream effects of hyperglycemia-induced retinal damage.