| Abstract: | Diabetes mellitus (DM), the 10th? leading cause of death worldwide, is a major and growing public health problem estimated to affect more than 578 million people in 2030 and 700 million people in 2045[1]. In diabetic animals, protein glycation and glucose autoxidation generate free radicals, which cause lipid peroxidation. Therefore, reactive oxygen species (ROS) can quickly accumulate, decrease antioxidant activity, and cause deterioration of kidney and liver function. A disrupted redox balance in cells also damages crucial biomolecules such as deoxyribonucleic acid (DNA), proteins and lipids. Oxidative stress (OS) is elevated in diabetes mellitus and may be a major factor in the development and evolution of the typical long-term pathophysiology of?diabetes?and?its?associated?complications[2]. |
