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

A case of mitochondrial enzymopathy, called also ophthalmoplegia plus, was observed in a 31-year-old man. Histoenzymatic investigations demonstrated in the myocytes decreased and irregularity of reactions for succinic dehydrogenase, tetrazole reductase and mitochondrial ATPase. In electron microscopy paracrystalline structures, lamellar bodies and concentrically condensed cristae were seen in the mitochondria, and increased glycogen stores outside the mitochondria.
Neurol Neurochir Pol
PMID:[A case of mitochondrial enzymopathy]. 297 67

Exposure of rats to elevated temperature of 28 degrees C or 35 degrees C for 3 days six hours daily resulted in a decreased rate of oxidation with succinate or glutamate + malate as substrates, by the mitochondria of liver. The higher decrease was observed in environment temperature of 35 degrees C. There was no change in ADP/O ratio. The activities of NADH: cytochrome c reductase and cytochrome oxidase were stimulated but activities of succinate dehydrogenase and succinate cytochrome reductase were decreased.
Acta Physiol Pol
PMID:Influence of increased environmental temperature on oxidation processes in rat liver mitochondria. 303 73

Using cytochemical methods the location and activity were determined of alkaline phosphatase, ATP-ase and succinate dehydrogenase as representative enzymes for the metabolic processes in neutrophils isolated from blood and cerebrospinal fluid (CSF) of patients with meningococcal meningoencephalitis as compared with peripheral blood neutrophils in a control group. The study showed presence of phosphatase on the membranes of many intracellular structures. The activity of the enzymes was higher than in the control group in the membranes of neutrophils in blood and CSF. This is explained as an effect of action of the chemotactic factor on the cell membrane and activation of the cell to movements and phagocytosis. ATP-ase activity in peripheral blood neutrophils in controls was found in all membranous structures in the cell. However, in peripheral blood neutrophils and CSF neutrophils in the acute stage of the disease the active enzyme was noted, in the first place, in cell membranes and digesting vacuoles, which reflected probably the direction of metabolic processes for phagocytosis and destroying of bacteria. The activity of succinate dehydrogenase was found in mitochondrial membranes. Peripheral blood and CSF neutrophils showed a high activity of the enzyme. In the CSF cells in acute phase atypical sites of succinate dehydrogenase activity were noted, which was explained as a sign of cell destruction.
Neurol Neurochir Pol
PMID:[Ultrastructural location of enzymes in peripheral blood neutrophils and in cerebrospinal fluid neutrophils in neuroinfections]. 832 38

The objective of this study was to analyse the effects of isoflurane anesthesia (lasting for 15 or 60 min) and isoflurane anesthesia termination (after 1 or 24 h) on met-enkephalin (MENK) and leu-enkephalin (LENK) levels in discrete brain areas and spinal cord segments in rabbits. Moreover histochemical analysis of activities of succinate dehydrogenase, magnesium-dependent adenosine triphosphatase (Mg++ATP-ase) and acid phosphatase in the striatum and hypothalamus were carried out to evaluate the effects of isoflurane anesthesia on energetic, transport and catabolic processes. Throughout anesthesia (15 and 60 min) and after its termination (1 h) the LENK contents were increased in hypothalamus, hippocampus, mesencephalon and lumbar segment of spinal cord. Moreover, during isoflurane anesthesia and after its termination (1 h) MENK and LENK levels decreased in cervical segment and MENK content dropped in thoracic segment of spinal cord. Histochemical data indicated, that isoflurane enhanced energetic processes as well as exchange processes in neurocytes, glial cells, capillary walls and ependymal cells of the third ventricle. Measurements of acid phosphatase activity provided evidence of no signs of toxicity of isoflurane in the examined areas. The changes in enkephalin levels observed during the isoflurane anesthesia and after its termination depended on the type of examined neuropeptides, as well as on parts of the brain and spinal cord studied. The changes observed after isoflurane administration in enkephalinergic system are discussed with regard to our earlier experiments with halothane and enflurane.
Pol J Pharmacol
PMID:Influence of isoflurane on enkephalin levels and on some indicatory enzymes in the central nervous system of rabbits. 943 56

The aim of this study was to evaluate the effect of 5-, 15-, and 60-min enflurane anesthesia on the levels of Met-enkephalin, Leu-enkephalin and neuropeptide Y in discrete areas of the rabbit brain. We also evaluated the effect of enflurane anesthesia on energetic, transport and catabolic processes by measuring the activities of succinate dehydrogenase, magnesium-dependent adenosine triphosphatase and acid phosphatase in the rabbit striatum and hypothalamus. Induction of anesthesia (5 min) decreased Met-enkephalin levels in the hypothalamus and striatum, and increased them in the hippocampus and mesencephalon. Induction of anesthesia increased Leu-enkephalin levels in all brain areas studied, except for the striatum, and increased neuropeptide Y content in the hippocampus. 15- and 60-min enflurane anesthesia increased Met-enkephalin content in the hypothalamus and hippocampus. After 15- and 60-min anesthesia, and after cessation of anesthesia, Leu-enkephalin levels were increased in the hypothalamus and mesencephalon, and were decreased in the striatum and hippocampus. In the striatum, neuropeptide Y content was significantly decreased during anesthesia and after cessation of anesthesia. Histochemical analysis revealed that enflurane enhanced ATP production, catabolic processes, and the rates of exchange and transport of energetic substrates in the striatum and hypothalamus. In conclusion, enflurane affects the levels of Met, Leu-enkephalins and NPY in a manner depending on the duration of anesthesia and the brain structure. Compared with isoflurane , which was studied in our previous study enflurane produces stronger alterations in the activities of enzymatic marker in the rabbit brain. This suggests that enflurane may be less safe than isoflurane.
Pol J Pharmacol
PMID:Effect of enflurane on selected neuropeptides and marker enzymes in rabbit brain. 1009 16

The hepatotoxic effect of 2,4-dichlorophenoxyacetic acid (2,4-D) was investigated. Ultrastructural changes were evaluated under a transmission electron microscope. Certain histoenzymatic reactions were examined (to acid phosphatase according to Gomori (AP) and to succinic dehydrogenase (SD) according to Nachlas) in parenchymal cells of the rat liver in acute intoxication induced by this herbicide. The experiment used 60 male Wistar rats divided into two groups: I-control--18 animals and II--42 animals which received chemically pure 2,4-D acid by gastric gavage in a dose of 200 mg/kg b.w. The animals were sacrificed after 12, 24, 48 hours and 4, 10 and 30 days of the experiment. The results indicate that the administration of 2,4-D acid to rats in a dose inducing acute intoxication leads to histoenzymatic and ultrastructural changes in the liver, which suggest nonspecific reversible adaptive-type damage to parenchymal cells. The changes observed indicate disorders in energetic processes in hepatocytes and are morphological exponents of intense detoxicative processes.
Mater Med Pol
PMID:Morphological changes in mitochondria and lysosomes of hepatocytes in acute intoxication with 2,4-dichlorophenoxyacetic acid (2,4-D). 1021 70

A number of data concerning the central action of mitochondrial toxins, substances impairing mitochondrial synthesis of ATP and thus compromising cellular energy status, has emerged within last years. 3-Nitropropionic acid (3-NPA) is an irreversible inhibitor of succinate dehydrogenase and mitochondrial complex II. The experimental administration of 3-NPA may lead to selective neuronal loss and chorea-like behavioral alterations but, as was recently shown, it also evokes clonic convulsions in rodents. The gathered data suggest that disturbed mitochondrial energy metabolism might initiate the chain of events culminating in seizure episode and that 3-NPA might become a useful tool in studying "mitochondrial" seizures. It has been hypothesized that the resistance to standard anticonvulsive therapy occurring among high proportion of epilepsy sufferers may result from the impairment of mitochondrial energy status due to either genetic predispositions or environmental influences.
Pol J Pharmacol
PMID:Seizures evoked by mitochondrial toxin, 3-nitropropionic acid: new mechanism of epileptogenesis? 1094 22

Mitochondrial dysfunction and abnormal electron chain transport (ECT) may be involved in the pathogenesis of ALS. The aim of this study was to investigate the effect of cerebrospinal fluid (CSF) from ALS patients on the activity of ECT enzymes in mitochondrial cerebral crude preparations in the rats. We found that CSF inhibited the activity of complex I-III in 20%, complex II-III in 12% and complex IV in 33% of the ALS patients. CSF from the controls did not affect the activity of complex I-III and II-III. The effect of the CSF ultrafiltrates with cut off below 5000 daltons on the activity of ECT enzymes was also investigated. The CSF ultrafiltrates inhibited the activity of complex I-III, complex II-III and complex IV in 38%, 44% and 53% of the ALS patients, and in 80%, 53% and 43% of the controls, respectively. The results of this study and our previously reported experiments on the sera of ALS patients may indicate that neurotoxic effects of body fluids from ALS patients could be mediated by inhibition of the respiratory chain enzymes. This confirms an important role of mitochondrial dysfunction in the pathogenesis of ALS.
Neurol Neurochir Pol 2001
PMID:[The role of mitochondrial respiratory chain in the pathogenesis of ALS]. 1173 84

3-Nitropropionic acid (3-NPA) is a mitochondrial toxin inhibiting the activity of succinate dehydrogenase. Its experimental application in rodents causes lesions of the striatum resembling the course of Huntington's disease in humans. Recently, we have shown that 3-NPA is also a potent convulsive and proconvulsive agent. This study investigated the effects of adenosine receptor agonists on neurodegeneration and convulsions induced by 3-NPA. Adenosinergic agonists prevented seizures but not striatal neuronal loss evoked by 3-NPA, what suggests that different mechanisms might contribute to these pathologies associated with application of mitochondrial toxin.
Pol J Pharmacol
PMID:Effect of adenosine receptor agonists on neurodegenerative and convulsive activity of mitochondrial toxin, 3-nitropropionic acid. 1178 16

Based on careful tissue processing, detailed structural analysis, and histochemical as well as cytophotometrical evaluation of the epidermis, the study presents data with respect to changes of tissue integrity during two storing modes (room temperature and 4 degrees C) and various storage times of the porcine auricle. Structural degeneration was first noted in the barrier region of the epidermis from where such changes spread, independent of storage conditions, from small horizontal necrotic islands and continuously with increasing storage time. The histochemical results corroborated these observations, emphasizing, however, that the lower epidermal layers seemed intact for a longer time period than the upper layers. Cytophotometrical evaluation of histochemical stainings showed, with regard to the enzyme succinate dehydrogenase, that oxidative metabolism was negatively affected in the early stages of storage, whereas epidermal lipids (neutral fats, glycolipids) remained relatively stable, even during storage at room temperature. In conclusion, it was obvious that the barrier region is the most sensitive element of the porcine ear epidermis. Taking into consideration that this part of the epidermis is most important for permeation studies, it seems reasonable to avoid any storage of porcine auricles at room temperature, and to use only auricles that have been stored at 4 degrees C for not more than 4 to 6 hours, immediately after delivery from the slaughter-house. In this way better tissue preservation can be achieved, whereby the use of shinkage-free water-soluble plastic embedding would generally improve the histological control of structural integrity, and the application of an easy to handle enzyme histochemical procedure (e.g. succinate dehydrogenase demonstration) to unfixed fresh-frozen sections would help to control basic aspects of tissue functions. The results are discussed in relation to the use of porcine integument as a model in human dermatological research.
Pol J Vet Sci 2003
PMID:The porcine ear skin as a model system for the human integument: influence of storage conditions on basic features of epidermis structure and function--a histological and histochemical study. 1267 65


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