Superoxide dismutase enhances recovery following myocardial ischemia

Burton, Karen P.

doi:10.1152/ajpheart.1985.248.5.h637

Cited by 59 publications

(37 citation statements)

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“…The evidence is based on the observed protective effect of superoxide dismutase [4] and/ or catalase 11, 2, 51 during ischemia and reperfusion. There are also reports that inhibition of the enzyme xanthine oxidase (a potential source of 0;) also affords protection to the ischemic myocardium [2, 31.…”

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The metabolic consequences of hydroperoxide perfusion on the isolated rat heart

Chatham

Gilbert

Radda

1989

European Journal of Biochemistry

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Perfusion of rat hearts with Krebs-Henseleit bicarbonate buffer containing low concentrations of hydrogen peroxide or t-butylhydroperoxide (50 -500 pM) caused an imbalance in the relative synthesis versus utilization rates of ATP, leading to a net hydrolysis of ATP and phosphocreatine. Hydrogen peroxide also caused an 80% inactivation of glyceraldehyde-3-phosphate dehydrogenase, resulting in an inhibition of glycolysis and a rapid accumulation of sugar phosphates as detected with 31P-NMR spectroscopy. This inhibition was partially reversiblc with peroxide-free perfusion, resulting in a cessation of high-energy-phosphate hydrolysis and a decrease in the accumulated inorganic phosphate and sugar phosphate. t-Butylhydroperoxide toxicity was irreversible. Providing an alternative, non-glycolytic substrate (butyrate) did not protect against the toxicity of hydrogen peroxide. but altered the relative importance of sugar phosphate formation versus ATP hydrolysis. Experiments with heart homogenates in vitro suggest that the inhibition of glyceraldehyde-3-phosphate dehydrogenasc is a consequence of a direct reaction of the enzyme with hydrogen peroxide or one of its metabolites. Hearts subjected to total global ischemia (1 0 -20 min), followed by reperfusion with oxygenated buffer, showed no detectable inactivation of glyceraldehyde-3-phosphate dehydrogenase, indicating that ischemia and reperfusion do not result in the production of high global concentrations of hydrogen peroxide.There is growing evidence that reactive oxygen species such as the superoxide anion (O;), hydrogen peroxide (H202) and the hydroxyl radical ('OH) are involved in reperfusion damage in the ischemic heart [I -51. The evidence is based on the observed protective effect of superoxide dismutase [4] and/ or catalase 11, 2, 51 during ischemia and reperfusion. There are also reports that inhibition of the enzyme xanthine oxidase (a potential source of 0;) also affords protection to the ischemic myocardium [2, 31. The highly reactive hydroxyl radical could be formed by the reaction between H 2 0 2 and 0; via the Fenton [6] and Haber-Weiss [7] reactions. It has been suggested that such reactions may take place under in viw conditions [8, 91. Despite a great deal of work it is still not clear where these reactive oxygen species are generated, in what quantity and what metabolic effects they may have. Despite reports that 0; and H 2 0 2 cause protein damage [lo, 1 I], these metabolites are considered relatively unreactive in the in vivo environment [12, 131. A more likely cause of damage is the highly reactive hydroxyl radical. In cellular systems it has been shown that the hydroxyl radical causes DNA strand breaks [XI and at high concentrations (2 mM) hydrogen peroxide produces leaky membranes [14]. The relevance of these experiments to reperfusion damage is unclear; by its very nature the damage resulting from reperfusion of the ischemic heart is rapid, whereas DNA and membrane damage take place over 30 min

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confidence: 99%

The metabolic consequences of hydroperoxide perfusion on the isolated rat heart

Chatham

Gilbert

Radda

1989

European Journal of Biochemistry

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“…CuZn-SOD has been reported to protect various organs from the damage caused by oxygen radicals (7,18,42). The uterine cervix, especially the region covered with stratified squamous epithelium, is at risk to high atmospheric oxygen tension.…”

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confidence: 99%

Immunohistochemical localization of CuZn-superoxide dismutase in human uterine cervix and cervical cancer.

Shiotani

Noda

Narimoto

et al. 1993

Acta Histochem. Cytochem

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“…It has been suggested that oxygen-derived free radicals may contribute to the myocardial injury associated with ischemia and reperfusion (1)(2)(3)(4)(5). Recently, using electron spin resonance (ESR) spectroscopy (6-15) and enhanced chemiluminescence (16), direct evidence of increased oxy gen-derived free radical production during reperfusion has been obtained.…”

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confidence: 99%