Proton and free oxygen radical interaction with the calcium transport system of cardiac sarcoplasmic reticulum

Heß, Michael; Okabe, Eiichiro; Kontos, Hermes A.

doi:10.1016/0022-2828(81)90258-3

Cited by 169 publications

(42 citation statements)

References 13 publications

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“…1,9 Moreover, decreased scavenging enzyme activity increases the generation of ROS and the compensatory mechanism of an increase in catecholamines in congestive heart failure also increases ROS. 20 The ROS themselves depress the activity of Ca 2+ binding and uptake by the sarcoplasmic reticulum, 21 which would lead to a decrease in cardiac contractility. The decrease in cellular pH during ischemia leads to formation of prostaglandins and leukotrienes, and ROS are produced during their synthesis.…”

Section: Discussionmentioning

confidence: 99%

Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Kishimoto

Shioji²,

Nakamura

et al. 2001

Jpn Circ J

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Section: Discussionmentioning

confidence: 99%

Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Kishimoto

Shioji²,

Nakamura

et al. 2001

Jpn Circ J

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“…Exogenous free radicals would be expected to enhance cellular calcium loading by the known inhibition ofNa'-K+ ATPase in the surface membrane and of Ca2+-ATPase in both the sarcolemma and the sarcoplasmic reticulum (20,22,23,(62)(63)(64)(65). Free radicals are also capable ofinjuring mitochondrial Ca2+-ATPase (34).…”

Section: Discussionmentioning

confidence: 99%

Glycolytic inhibition and calcium overload as consequences of exogenously generated free radicals in rabbit hearts.

Corretti¹,

Koretsune²,

Kusuoka³

et al. 1991

J. Clin. Invest.

105

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Free radicals have been implicated in the pathogenesis of reperfusion injury, but it is unclear how they exert their deleterious effects on cellular metabolism. Several lines of indirect evidence suggest that free radicals elevate intracellular Ca2" concentration ([Ca2"]) and inhibit glycolysis as part of their mechanism of injury. We tested these ideas directly in hearts subjected to hydroxyl radicals produced by the Fenton and Haber-Weiss reactions. Nuclear magnetic resonance spectra were obtained from Langendorff-perfused rabbit hearts before, during, and after 4 min of perfusion with H202 (0.75 mM) and Fe3+-chelate (0.1 mM). Isovolumic left ventricular pressure exhibited progressive functional deterioration and contracture after exposure to H202 + Fe3+. Phosphorus nuclear magnetic resonance (NMR) spectra revealed partial ATP depletion and sugar phosphate accumulation indicative of glycolytic inhibi-

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“…They observed that Ca2+-pump ATPase activity and steady-state Ca 2+ uptake were depressed by free radicals [129][130][131][132][133][134][135]. Direct measurement of the number and turnover of the pump units indicated that the number of the units was unchanged but turnover rate was decreased by oxygen free radicals [ 131 ].…”

Section: Ca2 § Processes Of Sarcoplasmic Reticulummentioning

confidence: 99%

“…Hess et al [129][130][131][132][133][134][135] have studied the effects of various types of oxygen free radical-generating systems on Ca 2 § transporting systems of cardiac sarcoplasmic reticulum. They observed that Ca2+-pump ATPase activity and steady-state Ca 2+ uptake were depressed by free radicals [129][130][131][132][133][134][135].…”

Section: Ca2 § Processes Of Sarcoplasmic Reticulummentioning

confidence: 99%

Oxygen free radicals and calcium homeostasis in the heart

et al. 1994

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Many experiments have been done to clarify the effects of oxygen free radicals on Ca 2+ homeostasis in the hearts. A burst of oxygen free radicals occurs immediately after reperfusion, but we have to be reminded that the exact levels of oxygen free radicals in the hearts are yet unknown in both physiological and pathophysiological conditions. Therefore, we should give careful consideration to this point when we perform the experiments and analyze the results.It is, however, evident that Ca 2+ overload occurs when the hearts are exposed to an excess amount of oxygen free radicals. Though ATP-independent Ca 2+ binding is increased, Ca 2+ influx through Ca 2 § channel does not increase in the presence of oxygen free radicals. Another possible pathway through which Ca 2. can enter the myocytes is Na+-Ca 2+ exchanger. Although, the activities ofNa § + ATPase and Na+-H + exchange are inhibited by oxygen free radicals, it is not known whether intracellular Na § level increases under oxidative stress or not. The question has to be solved for the understanding of the importance of Na § Ca z+ exchange in Ca 2+ influx process from extracellular space. Another question is 'which way does Na+-Ca 2+ exchange work under oxidative stress? Net influx or efflux of Ca 2 § ?' Membrane permeability for Ca 2+ may be maintained in a relatively early phase of free radical injury. Since sarcolemmal Ca2+-pumpATPase activity is depressed by oxygen free radicals, Ca 2 § extrusion from cytosol to extracellular space is considered to be reduced. It has also been shown that oxygen free radicals promote Ca 2 § release from sarcoplasmic reticulum and inhibit Ca 2+ sequestration to sarcoplasmic reticulum. Thus, these changes in Ca 2+ handling systems could cause the Ca 2+ overload due to oxygen free radicals. (Mol Cell Biochem 139: 91-100, 1994)

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Proton and free oxygen radical interaction with the calcium transport system of cardiac sarcoplasmic reticulum

Cited by 169 publications

References 13 publications

Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Serum Thioredoxin (TRX) Levels in Patients With Heart Failure

Glycolytic inhibition and calcium overload as consequences of exogenously generated free radicals in rabbit hearts.

Oxygen free radicals and calcium homeostasis in the heart

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