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)

Light microscopy was used to study rat lungs. Some morphological and biochemical characteristics after single bleomycin intratracheal administration in a dose of 10 mg/kg were studied. Some metabolic changes in the alveolar epithelium and vascular endothelium were estimated quantitatively. The peculiar picture of acute toxic alveolitis in the early stage of the injury and the features of fibrotic alveolitis by the 30-60th day were observed. The LDH and succinate dehydrogenase activities in the alveolar epithelium increased by the 3-7th day and returned to normal by the 30th day. At the same time the PL content increased 2-fold by the 30-60th day. The lysolecithin, sphingomyelin and phosphatidylserine concentration increased on the 3-7th day and returned to normal level on the 14th day. The phosphatidylglicerol content decreased significantly by the 60th day.
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PMID:[The structural changes in the lungs and the phospholipids of the pulmonary surfactant in experimental bleomycin-induced pneumosclerosis in rats]. 172 57

Activities of the following enzymes were assessed in cryostat sections of human embryonic and fetal placentae aged 7 to 22 weeks of the intrauterine life using the standard methods recommended by Lojda et al. (1978): alkaline phosphatase (AIP), and acid phosphatase (AcP), non-specific esterase (ANE), ATP-cleaving enzymes (ATP-ase), beta-glucuronidase, thiamine pyrophosphatase, dipeptidylaminopeptidase IV (DPP IV), aminopeptidase A and M (APA, APM), gamma-glutamyltransferase (GGT), glycero-3-phosphate dehydrogenase and succinate dehydrogenase (alpha-GPDH, SDH). Since week 7 high activity of AIP has been proved in the apical zone of the plasmodiotrophoblast. At the same time the DPP IV activity appeared in the plasmodiotrophoblast, in the stroma of villi, and, latter on, in vascular endothelium. In the fetal placenta the APA activity was pronounced both in the cytotrophoblast and the stroma of villi. The activities of AcP and ANE were relatively weak. In the course of development the activities of most enzymes were gradually increasing.
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PMID:Histochemistry of some enzymes in human embryonic and fetal placentae. 215 Oct 77

A previous study of endotoxemia in dogs demonstrated that exogenous prostacyclin (PGI2), normally a product of vascular endothelium, restored the cardiac index to normal and improved survival. To account for these results, a study was undertaken to test whether PGI2 would alter isolated rat or dog cardiac mitochondrial function following incubation with plasma from endotoxemic animals. A group of five animals served as anesthetized controls. A second group of seven mongrel dogs was given 1.75 mg Escherichia coli endotoxin/kg and was observed for 5 hours without treatment. Anesthesia did not alter cardiopulmonary function; however, 30 minutes after endotoxin administration, the cardiac index decreased from 148 +/- 25 (mean +/- SD) to 111 +/- 12 ml/kg . min (P less than 0.05) and further decreased to 89 +/- 20 ml/kg . min after 4 hours. Dog plasma obtained 2 to 5 hours after endotoxin infusion, incubated with rat or dog myocardial mitochondria, decreased succinate dehydrogenase (SDH) activity (P less than 0.05) and depressed mitochondrial respiration in the presence of the substrate succinate and adenosine diphosphate (ADP) from 180 to 87 Natoms oxygen/mg protein . min (P less than 0.05). There was no change in oxygen consumption when substrate alone was present, nor did plasma alter the amount of ADP phosphorylation as a function of oxygen consumption. A third group of seven animals, 30 minutes after administration of 1.75 mg endotoxin/kg, was treated with 100 ng/kg . min PGI2 for 3 hours. PGI2 infusion in this group prevented the decrease in cardiac index. Plasma obtained during and after PGI2 infusion did not decrease mitochondrial SDH activity, which remained higher than that in controls (P less than 0.001); mitochondrial respiration was also not altered. A correlation was observed between cardiac index and SDH activity (r = 0.58, P less than 0.001) and between cardiac index and mitochondrial respiration (r = 0.61, P less than 0.001). In PGI2-treated dogs cardiac mitochondria were functionally and structurally normal in contrast to the depression and disruption produced by endotoxemia, as observed by enzymatic assay as well as electron microscopy. These results suggest that endotoxemia depresses cardiac mitochondrial respiration, an event related to the decrease in cardiac index. In contrast, cardiac function and mitochondrial respiration are maintained with PGI2 treatment.
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PMID:Myocardial protection with prostacyclin after lethal endotoxemia. 704 19

Oxidative stress to vascular endothelium plays an important role in cold ischemia-reperfusion (CIR) injury. We compared mitochondrial and plasma membrane integrity in human endothelial cells after 20-min exposure to 500 microM H2O or 8-hr cold ischemia and simulated reperfusion. In both groups, plasma membrane integrity was maintained but respiration was significantly decreased, as measured by high-resolution respirometry. Uncoupling was more pronounced after H2O exposure compared with CIR. After H2O exposure, complex I respiration was significantly reduced, whereas CIR resulted additionally in a significant inhibition of complex II and IV respiration. Our results point to a partial overlap of the patterns of mitochondrial defects after H2O-mediated and CIR injury. In this respect, H2O exposure proved to be a useful model to study the mechanisms of CIR injury to human endothelial cells, whereas the full pattern of CIR injury could not be induced by a pulse of hydrogen peroxide exposure.
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PMID:H2O2-mediated oxidative stress versus cold ischemia-reperfusion: mitochondrial respiratory defects in cultured human endothelial cells. 1249 3

The metabolic changes in the homografted canine heart were studied in order to define the biochemical alterations accompanying homograft rejection. In several experiments, homograft rejection was accelerated by prior sensitization of the host animal. The homografted heart released pyruvate and lactate as well as malic dehydrogenase and aldolase. Extraction of glucose by the graft usually remained positive. During the accelerated rejection, the release of pyruvate and lactate was more pronounced, and even glucose appeared in increased concentrations in coronary vein blood. In many experiments the respiratory quotient of the transplanted heart as well as its glucose-oxygen extraction ratio were elevated. It seemed likely that the elevated respiratory quotients were the result of conversion of carbohydrates to fat, since the injection of thiamine hydrochloride resulted in further elevation of the respiratory quotient and in an increased myocardial pyruvate extraction. Apparently, thiamine corrected a metabolic block at the level of the cocarboxylase. The metabolic block or blocks present in the transplanted heart are likely to be the result of diminution in intracellular enzymes and coenzymes resulting from increased cellular permeability. The redox potential across the transplanted heart was positive, indicating the absence of anoxia. The results illustrate that glycolysis proceeds in the transplanted heart in the presence of oxygen. Histopathologic and histochemical studies show the earliest lesion to be an accumulation of lymphocytes around vessels at 3 hours. Swelling of vascular endothelium occurs. By 5 hours a polar perivascular cellular infiltrate of lymphocytes, plasma cells, macrophages, and histiocytes exists. Changes following at 19 hours show the appearance of Aschoff- and Anitschkow-like cells. Granulomatous myocarditis which was first perivascular became interstitial with lymphocytic and histiocytic invasion of the myocardium. After 8 days acceleration of swelling of vascular endothelium and granulomatous lesions were observed and necrosis of the myocardium was prominent. Endothelial hyperplasia occurred at 14 days. In the accelerated reaction these changes were intensified and necrosis began as early as 4 hours after grafting. Histochemical changes of DPNH diaphorase, lactic, malic, and succinic dehydrogenase showed only significant diminution of malic dehydrogenase in the cardiac muscle which was concurrent with the increase of this enzyme in the serum.
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PMID:Studies on the transplanted heart. Its metabolism and histology. 1387 18

The aim of the present investigation was to detect the regularities of postnatal development of "motor end-plate-muscle fiber (MF)-vascular network" system in different calf muscles of intact albino rats. Gastrocnemius, plantaris and soleus muscles were studied in 72 albino rats aged from 14 to 180 days. Identification of MF type was performed on the basis of succinate dehydrogenase and NADH-diaphorase activity. Cholinesterase activity of the neuro-muscular synapse (NMS) and alkaline phosphatase activity in the vascular endothelium were demonstrated using a combined histochemical method. The diameter of vascular network and the number of enzyme-active zones (EAZ) per one MF were the earliest parameters to be stabilized (before day 30). Histochemical profile of skeletal muscle was stabilized by the end of day 60. Dynamics of MF diameter and EAZ in NMS, vessel diameter and numbers per one MF is characterized by the periods of active changes (days 14-30), decrease (days 30-60) and stabilization (after day 60) of variance rate. The association between the level of oxidative metabolism and MF diameter was demonstrated.
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PMID:[Differentiation of calf skeletal muscles in the postnatal period of ontogenesis]. 2096 Jul 12