cytochrome c/infarkt

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Reduction of copper, zinc-superoxide dismutase in knockout mice does not affect edema or infarction volumes and the early release of mitochondrial cytochrome c after permanent focal cerebral ischemia.

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Copper,zinc-superoxide dismutase (SOD1) was shown to be highly protective against ischemia/reperfusion injury in the brain. We have recently reported that SOD1 prevents the release of mitochondrial cytochrome c and subsequent apoptosis after ischemia/reperfusion in mice. To investigate its dose

Diagnostic and Prognostic Utility of Circulating Cytochrome c in Acute Myocardial Infarction.

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BACKGROUND In contrast to cardiomyocyte necrosis, which can be quantified by cardiac troponin, functional cardiomyocyte impairment, including mitochondrial dysfunction, has escaped clinical recognition in acute myocardial infarction (AMI) patients. OBJECTIVE To investigate the diagnostic accuracy

Circulating p53 and cytochrome c levels in acute myocardial infarction patients.

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BACKGROUND Apoptosis causes myocardiocyte loss during and after myocardial infarction. Therapeutic approaches designed to arrest apoptosis would be a significant new development in the recovery of acute myocardial infarction (AMI). In order to examine apoptotic markers in the circulation, serum

FK506 reduces infarct volume due to permanent focal cerebral ischemia by maintaining BAD turnover and inhibiting cytochrome c release.

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It has been reported that immunosuppressant FK506 inhibited ischemic neuronal injury in forebrain ischemia or transient focal cerebral ischemia, but the mechanisms of the neuroprotective effect have not been clarified. In permanent focal cerebral ischemia, we investigated whether FK506 caused

[Determination of the concentration of cytochrome c and its antibodies in the blood serum for the diagnosis and prognosis of complications in myocardial infarct patients].

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EIA was used to demonstrate that the development of acute ischemia of the heart muscle progressing to necrosis is accompanied by an increase of the concentration of cytochrome c and antibodies against cytochrome c in the blood serum. As regards its specificity and sensitivity, the alteration in the

Circulating cytochrome c as potential biomarker of impaired reperfusion in ST-segment elevation acute myocardial infarction.

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In patients with ST-segment elevation acute myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI), abrupt reperfusion can induce myocardial injury and apoptotic cell death. Reperfusion-induced myocardial damage, however, cannot be easily evaluated in clinical

Cytochrome c release in acute myocardial infarction predicts poor prognosis and myocardial reperfusion on contrast-enhanced magnetic resonance imaging.

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BACKGROUND Myocardial ischemia and reperfusion injury in ST-segment elevation myocardial infarction (STEMI) can trigger no-flow, resulting in myocardial necrosis and apoptosis, even a poor prognosis. Cytochrome c can induce an apoptotic process. The aim of our study was to assess the relationship

Effects of Serum Cytochrome c on Contrast-Induced Nephropathy in Patients with ST-Elevation Myocardial Infarction Undergoing Percutaneous Coronary Intervention.

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Contrast-induced nephropathy (CIN) is a relatively infrequent complication after percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI). However, little is known about the association between cytochrome c (cyt c) and increased risk of CIN.

The effects of cytochrome C on the extent of myocardial infarction and regional function of the ischemic myocardium.

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The effects of cytochrome C, an electron carrier in the process of oxidative phosphorylation, on infarct size and regional left ventricular function after a coronary artery occlusion were investigated. Thus, in 30 dogs, 1 minute after left anterior descending coronary artery occlusion, 99mTc-labeled

Cytochrome-c detection: a diagnostic marker for myocardial infarction.

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Following a myocardial infarction (MI) cells die or are damaged and their contents leak into the blood circulation, resulting in elevated serum levels of various enzymes, proteins, and organic molecules. Over the past few decades, it has become standard practice to employ the detection of these

Cytochrome c oxidase III as a mechanism for apoptosis in heart failure following myocardial infarction.

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Cytochrome c oxidase (COX) is composed of 13 subunits, of which COX I, II, and III are encoded by a mitochondrial gene. COX I and II function as the main catalytic components, but the function of COX III is unclear. Because myocardial ischemia affects mitochondrial oxidative metabolism, we

Extent of mitochondrial hexokinase II dissociation during ischemia correlates with mitochondrial cytochrome c release, reactive oxygen species production, and infarct size on reperfusion.

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BACKGROUND The mechanisms by which ischemic preconditioning (IP) inhibits mitochondrial permeability transition pore opening and, hence, ischemia-reperfusion injury remain unclear. Here we investigate whether and how mitochondria-bound hexokinase 2 (mtHK2) may exert part of the cardioprotective

[Intracellular mechanisms of the effect of cytochrome C on various areas of the myocardium during the dynamic development of an experimental infarct].

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The effectiveness of the drug was shown to depend on the number of reversibly damaged cells. The intracellular mechanisms of cytochrome C effect are thought to be related to both the possibility of its permeation through the changed cell membrane of a cardiomyocyte and the action of the drug

[Effect of strophanthin and cytochrome C on myocardial contraction and the incidence of shock and ventricular fibrillation in experimental myocardial infarct].

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High ligation of the interventricular artery caused ventricular fibrillation in the first 2--4 minutes in 20% of cats. In the remaining animals myocardial contractility diminished to half its initial value. After that, contractility increased gradually. In cardiosclerosis myocardial contractility

[Cytochrome-C in the treatment of patients with acute myocardial infarct].

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Sixty-eight patients with acute macrofocal myocardial infarction were subdivided in two groups depending on the kind of treatment: routine (nitrates, beta-blocking agents, calcium antagonists) and cytochrom-C. It was found that cytochrom-C produced a positive effect on the indices of myoglobin and

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