Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic myocardium was produced by occluding the left circumflex coronary artery in anesthetized dogs. Autolyzed myocardium was produced by incubating transmural samples of canine left ventricle at 37 degrees C. Tissue pH was recorded continuously in each model using a microcombination pH electrode impaled into the midmyocardium. The activities of the five mitochondrial inner membrane enzyme complexes of electron transport and coupled oxidative phosphorylation were assayed as a function of time of ischemia or autolysis. While the activities of complex II (succinate-CoQ reductase) and IV (cytochrome c oxidase) were completely stable, that of complex I (NADH-CoQ reductase) decreased markedly, but largely only after 20 min of ischemia or autolysis. At 20 min and beyond, the decrease in the activity of complex I paralleled closely the decrease in whole mitochondrial oxygen uptake with NAD-linked substrates in both models. The activity of complex III (CoQH2-c reductase) decreased at a more gradual rate during ischemia or autolysis, and its rate of decrease paralleled that of succinate-supported oxygen uptake. The activity of complex V (oligomycin-sensitive ATPase) decreased most rapidly (by 40% in only 5 min of autolysis) but nearly leveled off beyond 20 min in the two models. A strikingly similar pattern of differential enzyme lability was observed in isolated control mitochondria incubated at lowered pH values. The results demonstrate 1) differential enzyme lability within the mitochondrial inner membrane, 2) a connection between severity of acidosis and the degree of enzyme activity loss, and 3) the usefulness of simple tissue autolysis as an analogue of in situ myocardial ischemia.
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PMID:Mitochondrial complexes I, II, III, IV, and V in myocardial ischemia and autolysis. 630 12

Histochemical and morphological changes in the tibial and calf muscles of the forelimbs were studied in dogs 3 months after experimentally induced ischemia of varying severity. In moderate ischemia, the activity of oxidation-reduction enzymes increases, that of adenozine triphosphatase decreases. The diameter of muscle fibers increases. These changes are considered to be compensatory. Severe ischemia is accompanied by suppressed activity of succinate dehydrogenase, myofibril damage, and formation of centres of ischemic dystrophy.
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PMID:[Changes in the skeletal muscles during experimental ischemia of the extremity]. 662 35

We describe two brothers, 25 and 19 years-old, with muscle pain and decreased strength after prolonged exercise; these symptoms are worsened by cold whether of fasting. One of the patients developed recurrent myoglobinuria and had one episode of renal failure. Laboratory investigations were normal between the crises, but during myoglobinuria, serum creatine kinase activity increased 100 times. Electromyography was suggestive of denervation. Muscle biopsy showed increased lipid droplets by the "oil red O" stain and increased activity of succinic dehydrogenase histochemical reaction. Lactate production during ischemia was normal. Biochemical analysis showed decreased carnitine-palmityl-transferase activity in muscle (7.23 and 10.58 nmoles/min/gr; normal range 66.7 +/- 17.3), with normal values for carnitine-octanoyl-transferase and carnitine-acetyl-transferase. The metabolic pathway of fatty acid utilization as an energy source for muscle during exercise in normal and in pathological conditions is discussed.
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PMID:[Myopathy due to carnitine palmitoyltransferase deficiency. Report of 2 cases with enzymatic analyses on muscle tissue]. 666 Nov 2

Hearts of 38 men dying suddenly of acute coronary insufficiency and autopsied within 3 hours after death were examined. Foci of acute ischemic injuries in different parts of the myocardium were studied by histochemical methods for which the activity of succinate dehydrogenase and phosphorylase were determined. Early ischemic lesions in the myocardium were found in 22 fatalities, of them 5 had acute myocardial infarction, in 9 foci of ischemia were combined with the presence of postinfarction scars and fine focal cardiosclerosis, in 8 cases foci of early ischemia were the only changes in the myocardium. The majority of the decreased had stenosing atherosclerosis of the coronary arteries. Localization of ischemia foci in the myocardium did not always correspond to the severity of stenosing or the presence of thrombosis of the artery supplying the corresponding parts of the heart muscle. No foci of ischemia in the myocardium were found in 16 decreased who also had quite marked coronary atherosclerosis.
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PMID:[Early ischemic injuries of the myocardium in sudden cardiac death]. 742 69

The initiating factor in ARDS is a matter of controversy. Some investigators relate ARDS development to diffuse pulmonary microemboli after stress ranging from sepsis to non-thoracic and thoracic trauma. Others indicate hyperoxic exposure as the causative agent. This investigation looked for a common factor in ischemia and hyperoxic exposure in lung which could cause the genesis of ARDS. Studies of oxidative phosphorylation, succinate dehydrogenase activity and ATP level were performed on ischemic and 100% O2 exposed lung. Results in both showed decreased respiration rate below the basal rate, decreased SDH activity, followed by marked decrease in ATP levels in pulmonary tissue. Decrease in respiration (ATP production) capacity and ATP levels in ischemic lung were such that normal cell functions could not be sustained if returned to normal circulation. Hyperbaric O2 therapy would subsequently decrease energy metabolism in regions of normal circulation and in previously ischemic regions.
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PMID:A common denominator in the etiology of adult respiratory distress syndrome. 743 54

Examinations of plastic function changes in myocardial cells (MC) from 36 patients with chronic ischemic heart disease were carried out before, during and soon after cardioplegic ischemia. The initial mean number of silver grains in nucleoli varied greatly showing some difference between groups of the patients with (9.5 +/- 0.48) or without (11.0 +/- 0.5) myocardial infarction. During the myocardial arrest this index of MC plastic activity was decreased in all but 7 patients. In contrast to this, it was elevated in most patients tested during subsequent reperfusion. On the basis of these data and parallel histochemical photometric assessment of DNA, RNA and succinate dehydrogenase activity, a hypothesis was suggested which explains the non-standard elevation of ribosomal cistron activity during both myocardial arrest and reperfusion by their compensatory reaction to myocardial injury.
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PMID:[An evaluation of the plastic function of the cardiomyocytes by silver staining of the nucleoli in patients operated on for ischemic heart disease]. 752 67

Acute interruption of arterial blood flow to the extremities is often associated with significant morbidity and mortality. Broad-spectrum mitogenic and non-mitogenic activities of FGFs inspired us to study its protecting effects on tissue injuries in ischemia reperfusion condition. We found that systemic administration of aFGF after reperfusion onset prevented severe skeletal muscle injuries. In rats treated with aFGF, the tissue edema was reduced significantly, the tissue viability was increased, and the muscle fibers contained more succinate dehydrogenase (SDH) and adenosine triphosphatase (ATPase). The pathological results supported the concept of improved prevention with aFGF treatment. The possible tissue protection by aFGF may come from its ability to regulate the concentration of extra- and intracellular calcium ion. Besides, it may moderate other Ca2+ dependent enzyme conversion processes. Also, it may take part in the vascular tone regulation under ischemia and reperfusion conditions. These results suggest further study of tissue ischemia prevention with FGF and its possible mechanisms in the future.
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PMID:Acidic fibroblast growth factor reduces rat skeletal muscle damage caused by ischemia and reperfusion. 754 Sep 68

The CA1 region of hippocampus is selectively vulnerable to a variety of insults, including hypoxia-ischemia and Alzheimer's disease, but the basis of this regional susceptibility is poorly understood. We examined the regional hippocampal sensitivity to mitochondrial metabolic disruption induced by malonate, an inhibitor of succinate dehydrogenase. The CA1 region was exquisitely sensitive to malonate and the dentate gyrus was extremely resistant; the CA3 region had intermediate sensitivity. This pattern of vulnerability is reminiscent of hypoxic-ischemic damage. Malonate damage was blocked by the N-methyl-D-aspartic acid (NMDA) antagonist, MK-801, but regional susceptibility to malonate did not correlate with the density of NMDA receptors. Instead, malonate toxicity was inversely correlated with activity of succinate dehydrogenase. Our results suggest that regional metabolic capacity may help to determine sensitivity to metabolic/excitotoxic insults such as hypoxia-ischemia.
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PMID:Selective vulnerability of the CA1 region of hippocampus to the indirect excitotoxic effects of malonic acid. 767 3

Electron transport and production of O2-/H2O2 by the NADH dehydrogenase flavin-semiquinone (FMNH.) and ubisemiquinone (UQH.) were studied in a model of in vivo ischemia-reperfusion in rat kidney. H2O2 production rates were assessed in isolated mitochondria using either succinate, with and without antimycin, or malate-glutamate, with and without rotenone. Respiratory activities of isolated mitochondria and activity of NADH- and succinate-cytochrome c reductase and of NADH- and succinate-dehydrogenase in submitochondrial particles were measured to evaluate the electron flux throughout respiratory carriers. The mitochondrial H2O2 production rate was approximately 1.5- and 4-times increased in ischemic and ischemic-reperfused kidneys, respectively. Ischemia caused a marked decrease in the electron transport throughout the NADH-UQ segment with no significant changes either in the NADH dehydrogenase activity or in the electron flux trough the succinate-cytochrome oxidase segment. Reperfusion did not further affect the NADH-ubiquinone segment but markedly inhibited the succinate-supported oxygen consumption, succinate-cytochrome c reductase and succinate dehydrogenase activity. Our results show a redistribution of the electron flux with an increased rate of superoxide anion/hydrogen peroxide production at NADH dehydrogenase in mitochondria subjected to ischemia only. After 10 min reperfusion an impairment of the electron flow at succinate-cytochrome c segment is established and hydrogen peroxide production by UQH. increases up to maximal values becoming the major source of superoxide anion/hydrogen peroxide.
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PMID:Mitochondrial sites of hydrogen peroxide production in reperfused rat kidney cortex. 772 10

The influence of dietary n-6 and n-3 polyunsaturated fatty acids (PUFA) on heart pump function and mitochondrial energy metabolism was investigated before and after ischemia. Weanling male Wistar rats were fed for 8 weeks a diet containing either 10% of sunflower seed oil (SSO group) or 10% of a 1:1 (w/w) mixture of fish oil and sunflower seed oil (FO group). The hearts were perfused according to the working mode for 15 min with a Krebs-Henseleit medium containing glucose (11 mM), insulin (10 IU/L) and caprylic acid (25 microM). They were then either maintained in normoxic conditions (70 min) or subjected to a global no-flow normothermic ischemia (20 min) followed by reperfusion (50 min). The aortic and coronary flows were monitored at 5-min intervals. The lactate dehydrogenase (LDH) release in the coronary effluent was evaluated in the control hearts and during ischemia/reperfusion. At the end of the perfusion, two subpopulations of mitochondria were prepared from each heart, by either mechanical or enzyme extraction (ME and EE mitochondria, respectively). The succinate dehydrogenase (SDH) activity was evaluated. Furthermore, the respiration parameters were assessed with either glutamate (20 mM) or palmitoylcarnitine (25 microM) as substrate. Substituting sunflower seed oil by fish oil in the diet provoked a large decrease in the n-6/n-3 PUFA ratio of cardiac phospholipids. The n-3 PUFA enrichment did not alter the coronary and aortic flows nor the LDH release in physiological conditions. Conversely, during post-ischemic reperfusion, the increased amount of n-3 PUFA improved the recovery of aortic flow and decreased the LDH release, without affecting significantly the coronary flow. In ME and EE mitochondria, the phospholipid n-6/n-3 PUFA ratio was similarly modified by the dietary manipulations. The analysis of total cardiac SDH activity suggested an ischemia-induced oedema, of similar magnitude in the two dietary groups. However, neither dietary manipulations nor ischemia influenced the mitochondrial extraction. Similarly, the parameters of glutamate oxidation were also unaffected. Conversely, with palmitoylcarnitine, post-ischemic reperfusion induced a decrease in both state III respiration rate and energy production which were more important in the EE mitochondria of the SSO group. These results suggest that the recovery of mitochondrial energy metabolism and myocardial pump function during reperfusion may be improved in n-3 PUFA-rich hearts. This could be related to a lower injury in n-3 PUFA-rich membranes. Since cardiac function in physiological conditions was not affected by the diet, fish oil could be considered as a beneficial factor to limit heart injury during ischemia and reperfusion.
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PMID:Influence of the phospholipid n-6/n-3 polyunsaturated fatty acid ratio on the mitochondrial oxidative metabolism before and after myocardial ischemia. 791 84


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