Abstract
Creatine Phosphokinase (CK) release is commonly used to assess myocardial damage in laboratory models as well as clinically. At least part of the myocardial damage observed during reoxygenation of the heart appears to be mediated by superoxide produced by xanthine oxidase.1 While many reports have shown protection of reoxygenated myocardium by superoxide dismutase (SOD), occasional reports fail to observe protection by SOD.2 When we examined CK release by the continuously perfused anoxic/reoxygenated rat heart we saw marked protection by SOD;1 when we varied the model and examined the rat heart subjected to global no-flow ischemia/reperfusion, we saw an apparent paradoxical exacerbation of CK release in the presence of SOD, as described below. This led us to examine the possibility that SOD might, in fact, protect CK from partial inactivation by O -2 .
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References
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© 1988 Plenum Press, New York
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McCord, J.M., Russell, W.J. (1988). Inactivation of Creatine Phosphokinase by Superoxide during Reperfusion Injury. In: Simic, M.G., Taylor, K.A., Ward, J.F., von Sonntag, C. (eds) Oxygen Radicals in Biology and Medicine. Basic Life Sciences, vol 49. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5568-7_141
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DOI: https://doi.org/10.1007/978-1-4684-5568-7_141
Publisher Name: Springer, Boston, MA
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