Oxidative stress and erectile dysfunction (ED) are closely linked, with oxidative stress playing a significant role in the pathophysiology of ED. This review explores the mechanisms by which oxidative stress contributes to ED, including its impact on endothelial function, nitric oxide (NO) signaling, and vascular health. Key factors contributing to oxidative stress include aging, diabetes, hypertension, hyperlipidemia, smoking, obesity, alcohol consumption, and psychological stress. Reactive oxygen species (ROS) are generated by various sources such as NADPH oxidase, xanthine oxidase, uncoupled endothelial NO synthase (eNOS), and mitochondrial electron transport. These ROS impair NO availability, leading to endothelial dysfunction, reduced vasodilation, and increased vascular tone, all of which contribute to ED. Additionally, ROS can damage nitrergic neurons and reduce the signaling of neuronal NO synthase (nNOS), further exacerbating ED. Therapeutic approaches targeting oxidative stress, including antioxidants and lifestyle modifications, show promise in alleviating ED symptoms. The review emphasizes the need for further research to develop effective treatments, highlighting the interplay between oxidative stress and vascular health in ED. Integrating pharmacological and non-pharmacological strategies could enhance clinical outcomes for ED patients, advocating for oxidative stress management in ED treatment protocols to improve patient quality of life.Oxidative stress and erectile dysfunction (ED) are closely linked, with oxidative stress playing a significant role in the pathophysiology of ED. This review explores the mechanisms by which oxidative stress contributes to ED, including its impact on endothelial function, nitric oxide (NO) signaling, and vascular health. Key factors contributing to oxidative stress include aging, diabetes, hypertension, hyperlipidemia, smoking, obesity, alcohol consumption, and psychological stress. Reactive oxygen species (ROS) are generated by various sources such as NADPH oxidase, xanthine oxidase, uncoupled endothelial NO synthase (eNOS), and mitochondrial electron transport. These ROS impair NO availability, leading to endothelial dysfunction, reduced vasodilation, and increased vascular tone, all of which contribute to ED. Additionally, ROS can damage nitrergic neurons and reduce the signaling of neuronal NO synthase (nNOS), further exacerbating ED. Therapeutic approaches targeting oxidative stress, including antioxidants and lifestyle modifications, show promise in alleviating ED symptoms. The review emphasizes the need for further research to develop effective treatments, highlighting the interplay between oxidative stress and vascular health in ED. Integrating pharmacological and non-pharmacological strategies could enhance clinical outcomes for ED patients, advocating for oxidative stress management in ED treatment protocols to improve patient quality of life.