Obesity is a chronic, multifactorial disease characterized by excessive accumulation of body fat. Adipose tissue, beyond its role in fat storage, secretes adipokines, which regulate metabolism and energy homeostasis. However, obesity is associated with increased production of reactive oxygen species (ROS), leading to oxidative stress (OS), which contributes to inflammation and metabolic disorders. Adipokines such as leptin, TNF-α, IL-6, adiponectin, resistin, and visfatin play key roles in metabolic regulation, but their dysregulation can promote insulin resistance, inflammation, and atherosclerosis. Obesity also increases the risk of endothelial dysfunction, characterized by reduced nitric oxide (NO) availability and increased vascular inflammation. Mechanisms underlying OS in obesity include mitochondrial dysfunction, fatty acid oxidation, increased oxygen consumption, and dietary factors. Obesity is linked to reduced antioxidant capacity, which exacerbates OS and its associated health consequences, including cardiovascular disease, diabetes, and metabolic syndrome. Antioxidant supplementation may help mitigate these effects. Inflammation is a key component of obesity, with adipose tissue acting as a chronic inflammatory source. Endothelial dysfunction, a result of OS and inflammation, is a major contributor to cardiovascular complications in obesity. Effective prevention and management strategies for obesity-related OS and metabolic disorders require a comprehensive understanding of these mechanisms and the development of targeted interventions.Obesity is a chronic, multifactorial disease characterized by excessive accumulation of body fat. Adipose tissue, beyond its role in fat storage, secretes adipokines, which regulate metabolism and energy homeostasis. However, obesity is associated with increased production of reactive oxygen species (ROS), leading to oxidative stress (OS), which contributes to inflammation and metabolic disorders. Adipokines such as leptin, TNF-α, IL-6, adiponectin, resistin, and visfatin play key roles in metabolic regulation, but their dysregulation can promote insulin resistance, inflammation, and atherosclerosis. Obesity also increases the risk of endothelial dysfunction, characterized by reduced nitric oxide (NO) availability and increased vascular inflammation. Mechanisms underlying OS in obesity include mitochondrial dysfunction, fatty acid oxidation, increased oxygen consumption, and dietary factors. Obesity is linked to reduced antioxidant capacity, which exacerbates OS and its associated health consequences, including cardiovascular disease, diabetes, and metabolic syndrome. Antioxidant supplementation may help mitigate these effects. Inflammation is a key component of obesity, with adipose tissue acting as a chronic inflammatory source. Endothelial dysfunction, a result of OS and inflammation, is a major contributor to cardiovascular complications in obesity. Effective prevention and management strategies for obesity-related OS and metabolic disorders require a comprehensive understanding of these mechanisms and the development of targeted interventions.