The copper‐zinc superoxide dismutase activity in selected diseases

Abstract

Copper‐zinc superoxide dismutase (Cu,Zn‐SOD) plays a protective role in various types of tissue protecting them from oxidative damage. Alterations in Cu,Zn‐SOD (SOD1 and SOD3) activity and its expression have been observed in pathological occurrences most prevalent in modern society, including inflammatory bowel disease, obesity and its implications—diabetes and hypertension, and chronic obstructive pulmonary disease. Moreover, several SOD1 and SOD3 gene polymorphisms have been associated with the risk of developing a particular type of disease, or its exacerbation. This article features recent observations in this topic, aiming to show the importance of proper gene sequence and activity of Cu,Zn‐SOD in the aforementioned diseases.

Paeonol Attenuates Methotrexate-Induced Cardiac Toxicity in Rats by Inhibiting Oxidative Stress and Suppressing TLR4-Induced NF-κB Inflammatory Pathway

“…GSH, a tripeptide nonenzymatic antioxidant, performs an essential role in antioxidant protection directly via scavenging ROS and indirectly via working as a cofactor of antioxidant enzymes [43]. SOD, an important first line antioxidant enzyme, catalyzes the dismutation of the superoxide radical into either molecular oxygen or hydrogen peroxide [44]. The inhibitory effect of paeonol on lipid peroxidation, assessed as MDA, could be secondary to its antioxidant activity and/or its repressing effect on inducible NO synthase-(iNOS-) mediated NO bioavailability [45,46].…”

Oxygenic metabolism in nutritional obesity induced by olive oil. The influence of vitamin C

“…77,78 Obesity is an important problem in modern society and is associated with oxidative stress. 79 One of the main sources of oxidative stress in obesity is altered lipid homeostasis. In addition, ROS production is a consequence of free fatty acid oxidation.…”

Alterations in Concentration/Activity of Superoxide Dismutases in Context of Obesity and Selected Single Nucleotide Polymorphisms in Genes: SOD1, SOD2, SOD3

“…Interestingly, despite the fact that two of three mentioned SODs are ascribed to the intracellular compartment, it is known that all of them could be found in the extracellular compartment (serum, plasma), which is assumed to be due to migration of intracellular isozymes SOD1 and SOD2 to the extracellular matrix [27][28][29]. The association of SOD with obesity is due to its protective role as an antioxidant [30]. The extracellular SOD, SOD3, due to its abundance on the surface of endothelium, neutralizes the superoxide anion in the extracellular matrix, disrupting the generation of peroxynitrite, one of the mediators of pancreatic β-cell damage [31].…”