Superoxide Dismutase

McCord, Joe M.; Fridovich, Irwin

doi:10.1016/s0021-9258(18)63504-5

Cited by 11,360 publications

(792 citation statements)

References 31 publications

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“…Since their discovery by Joe McCord and Irwin Fridovich [3], their role as a major antioxidant defensehas been firmly recognized [4]. The work by I. Fridovich and collaborators was crucial in defining the role of oxidant/antioxidant processes in ischemia/reperfusionassociated pathologies in humans and animal models [5,6].…”

Section: Introductionmentioning

confidence: 99%

Superoxide Dismutase Administration: A Review of Proposed Human Uses

et al. 2021

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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.

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Section: Introductionmentioning

confidence: 99%

Superoxide Dismutase Administration: A Review of Proposed Human Uses

et al. 2021

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“…The increase of ROS is an important characteristic of LIRI, which makes a key contribution to pulmonary failure (Sun et al, 2011). Importing anti-oxidants to balance the production of ROS is an important strategy to reduce the toxicity caused by excessive ROS (McCord and Fridovich, 1969). As a main anti-oxidant in the body, SOD can catalyze the conversion of superoxide to oxygen and hydrogen peroxide, which will be converted into water and oxygen by other anti-oxidant proteins including thioredoxin, catalase and glutathione peroxidase (Wang et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Kaempferol Alleviates Oxidative Stress and Apoptosis Through Mitochondria-dependent Pathway During Lung Ischemia-Reperfusion Injury

Chen

Yang

et al. 2021

Front. Pharmacol.

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In previous study, we reported that kaempferol ameliorates significantly lung ischemia-reperfusion injury (LIRI), and may be achieved by targeting the SIRT 1 pathway. This study further explored the anti-LIRI mechanism of kaempferol. In vitro, the rat alveolar epithelial cells L2 was cultured and subjected to anoxia/reoxygenation (A/R) insult. In vivo, SD rats were operated to establish LIRI model. The related indicators of oxidative stress and apoptosis in L2 cells and rats lung tissues were detected. Results showed that kaempferol pre-treatment significantly increased the cell viability, improved mitochondrial membrane potential, inhibited the opening of mitochondrial permeability transition pores, reduced the levels of oxidative stress and apoptosis, increased the expressions of Bcl-2 and mitochondrial cytochrome c, and decreased the expressions of Bax and cytoplasmic cytochrome c in L2 cells after A/R insult. In vivo, kaempferol improved the pathological injury, inhibited the levels of oxidative stress and apoptosis, increased the expressions of Bcl-2 and mitochondrial cytochrome c, and decreased the expressions of Bax and cytoplasmic cytochrome c in rats lung tissues after I/R. However, the aforementioned effects of kaempferol were significantly attenuated by the SIRT 1 inhibitor EX527 or the PGC-1α inhibitor SR-18292. What’s more, SR-18292 has not reversed the effect of kaempferol on increasing the protein activity of SIRT 1. Above results suggest that kaempferol ameliorates LIRI by improving mitochondrial function, reducing oxidative stress and inhibiting cell apoptosis. Its molecular mechanism of action includes the SIRT 1/PGC-1α/mitochondria signaling pathway.

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“…SOD activity was measured according to McCord and Fridovich [29], adapted to microplate, using the xanthine/xanthine oxidase mediated reduction of cytochrome C. Briefly, 100 µL of 50 mM phosphate buffer (pH 7.8) was added to 50 µL of PMS sample in each microplate well, followed by the addition of 50 µL of 0.14 mM xanthine, 50 µL of 60 mM cytochrome C, and 50 µL of 10 mU mL −1 xanthine oxidase. The decrease of the cytochrome C reduction was followed at 550 nm for 10 min, and SOD activity was expressed in U mg −1 of protein using a SOD standard of 1.5 U mL −1 , where 1 U represents the amount of enzyme required to inhibit the rate of reduction of cytochrome C by 50%.…”

Section: Antioxidant and Detoxification Defensesmentioning

confidence: 99%

Asparagopsis armata Exudate Cocktail: The Quest for the Mechanisms of Toxic Action of an Invasive Seaweed on Marine Invertebrates

Silva

Simões

Félix

et al. 2021

Biology

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The seaweed Asparagopsis armata exhibits a strong invasive behavior, producing halogenated compounds with effective biological effects. This study addresses the biochemical responses to sublethal concentrations of A. armata exudate on the marine snail Gibbula umbilicalis whole body and the shrimp Palaemon elegans eyes and hepatopancreas. Antioxidant defenses superoxide dismutase (SOD) and glutathione-S-transferase (GST), oxidative damage endpoints lipid peroxidation (LPO) and DNA damage, the neuronal parameter acetylcholinesterase (AChE), and the fatty acid profile were evaluated. Results revealed different metabolic responses in both species. Despite previous studies indicating that the exudate affected G. umbilicalis’ survival and behavior, this does not seem to result from oxidative stress or neurotoxicity. For P. elegans, the inhibition of AChE and the decrease of antioxidant capacity is concomitant with the increase of LPO, suggesting neurotoxicity and oxidative stress as contributor mechanisms of toxicity for this species. Fatty acid profile changes were more pronounced for P. elegans with a general increase in polyunsaturated fatty acids (PUFAs) with the exudate exposure, which commonly means a defense mechanism protecting from membrane disruption. Nonetheless, the omega-3 PUFAs arachidonic acid (ARA) and docosapentaenoic acid (DPA) increased in both invertebrates, indicating a common regulation mechanism of inflammation and immunity responses.

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Superoxide Dismutase

Cited by 11,360 publications

References 31 publications

Superoxide Dismutase Administration: A Review of Proposed Human Uses

Superoxide Dismutase Administration: A Review of Proposed Human Uses

Kaempferol Alleviates Oxidative Stress and Apoptosis Through Mitochondria-dependent Pathway During Lung Ischemia-Reperfusion Injury

Asparagopsis armata Exudate Cocktail: The Quest for the Mechanisms of Toxic Action of an Invasive Seaweed on Marine Invertebrates

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