Abstract
Oxidative stress (OS) is defined as a disturbance in the prooxidant-antioxidant balance of the cell, in favor of the former, which results in the antioxidant capacity of the cell to be overpowered. Excess reactive oxygen species (ROS) production is very harmful to cell constituents, especially proteins, lipids, and DNA, thus causing damage to the cell. Oxidative stress has been associated with a variety of pathologic conditions, including diabetes mellitus (DM), cancer, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and accelerated aging. Regarding DM specifically, previous experimental and clinical studies have pointed to the fact that oxidative stress probably plays a major role in the pathogenesis and development of diabetic complications. It is postulated that hyperglycemia induces free radicals and impairs endogenous antioxidant defense systems through several different mechanisms. In particular, hyperglycemia promotes the creation of advanced glycation end-products (AGEs), the activation of protein kinase C (PKC), and the hyperactivity of hexosamine and sorbitol pathways, leading to the development of insulin resistance, impaired insulin secretion, and endothelial dysfunction, by inducing excessive ROS production and OS. Furthermore, glucose variability has been associated with OS as well, and recent evidence suggests that also hypoglycemia may be playing an important role in favoring diabetic vascular complications through OS, inflammation, prothrombotic events, and endothelial dysfunction. The association of these diabetic parameters (i.e., hyperglycemia, glucose variability, and hypoglycemia) with oxidative stress will be reviewed here.
Highlights
Oxidative stress (OS) is defined as a disturbance in the prooxidant-antioxidant balance of the cell, in favor of the former, so that the antioxidant capacity of the cell is overcome [1, 2], potentially leading to tissue injury [3]
Recent data made available by the International Diabetes Federation (IDF) indicate that 463 million people were diagnosed with diabetes worldwide in 2019, and it is estimated that this number will increase to 700 million by 2045, the preponderance of who will be diagnosed with type 2 diabetes (T2D) [35]
Various mechanisms associated with hyperglycemia, such as the production of advanced glycation end-products (AGEs), the activation of protein kinase C (PKC), the accumulation of sorbitol, and the hyperactivity of the hexosamine pathway, lead to reactive oxygen species overproduction and a decrease in the endogenous antioxidant defense systems
Summary
Oxidative stress (OS) is defined as a disturbance in the prooxidant-antioxidant balance of the cell, in favor of the former, so that the antioxidant capacity of the cell is overcome [1, 2], potentially leading to tissue injury [3]. It has been claimed that the α-tocopherol form is the most important lipid-soluble antioxidant and that it protects membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction. This removes the free radical intermediates and prevents the propagation reaction from continuing. ROS and RNS are typically created by firmly controlled enzymes, and their overproduction results in a harmful process (oxidative distress) that can be a central mediator of injury to cell constituents, including lipids and membranes, proteins, and DNA. This review will examine the available evidence for the association between diabetes mellitus and oxidative stress, and especially the individual contribution of the three glycemic indices (hyperglycemia, glucose variability, and hypoglycemia) on the maintenance of “redox homeostasis” in people with diabetes and their involvement in the pathogenesis of diabetic complications
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