Abstract
Superoxide dismutases (SODs) are metalloenzymes that play a major role in antioxidant defense against oxidative stress in the body. SOD supplementation may therefore trigger the endogenous antioxidant machinery for the neutralization of free-radical excess and be used in a variety of pathological settings. This paper aimed to provide an extensive review of the possible uses of SODs in a range of pathological settings, as well as describe the current pitfalls and the delivery strategies that are in development to solve bioavailability issues. We carried out a PubMed query, using the keywords “SOD”, “SOD mimetics”, “SOD supplementation”, which included papers published in the English language, between 2012 and 2020, on the potential therapeutic applications of SODs, including detoxification strategies. As highlighted in this paper, it can be argued that the generic antioxidant effects of SODs are beneficial under all tested conditions, from ocular and cardiovascular diseases to neurodegenerative disorders and metabolic diseases, including diabetes and its complications and obesity. However, it must be underlined that clinical evidence for its efficacy is limited and consequently, this efficacy is currently far from being demonstrated.
Highlights
We carried out a PubMed query, using the keywords “Superoxide dismutases (SODs)”, “SOD mimetics”, “SOD supplementation”, which included papers published in the English language, between 2012 and 2020, on the potential therapeutic applications of SODs, including detoxification strategies
Superoxide dismutases (SODs) are metalloenzymes found in eukaryotes and some prokaryotes and as shown in Figure 1A, they are localized in the cytosol and the mitochondrial intermembrane (Cu, Zn-SOD or SOD1), the mitochondrial matrix and inner membrane (Mn-SOD or SOD2) [1], and extracellular compartment (Cu, Zn-SOD or SOD3) [2]
The activation of the phosphoinositide 3-kinase (PI3K)/AKT axis inversely regulates the distribution of Nuclear Factor (NF)-κB and FOXO transcription factors; FOXO factors are phosphorylated and displaced from the nucleus to the cytoplasm, while NF-κB translocates to the nucleus, activating antioxidant genes, including SODs [50]
Summary
Superoxide dismutases (SODs) are metalloenzymes found in eukaryotes and some prokaryotes and as shown in Figure 1A, they are localized in the cytosol and the mitochondrial intermembrane (Cu, Zn-SOD or SOD1), the mitochondrial matrix and inner membrane (Mn-SOD or SOD2) [1], and extracellular compartment (Cu, Zn-SOD or SOD3) [2]. SOD catalyzes the conversion of the superoxide anion free radical ( O2 − ) to hydrogen peroxide (H2 O2 ) and molecular oxygen O2 (Figure 1A,B). Low and diminished SOD activity protecting, and high doses (50 μg/mL perfusate) exacerbating has been associated with a significant riskinofthe oxidative stress, resulting inreoxygenationdisease, such injury [10]. Bovine SOD, known as orgotein, was usually preferred It can be limited by its intramuscular administration, administration frequency (2~3 times weekly) [9], and possible toxicity, caused by the presence of 20% impurities (albumin and chymotrypsin are the primary contaminants), in the pharmaceutical preparation that may result in immediate hypersensitivity reactions [18], and other side effects, including allergy [16]. We carried out a PubMed query starting with the keywords “SOD”, “SOD mimetics”, and “SOD supplementation” that included papers published in the English language, between 2012 and 2020, on the potential therapeutic applications of SOD, including detoxification strategies
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