Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Intravitreal injection of 5 micrograms of Shigella endotoxin, in the rabbit eye, induced an acute inflammatory response which was characterised by conjunctival hyperaemia, limbal and ciliary vascular injection, iritis, aqueous flare, miosis and reduction in intraocular pressure. Iris-ciliary body tissues, from normal and inflamed eyes, were fractionated into subcellular enriched fractions and the activities and distribution of selected enzymes were estimated. Alkaline phosphatase, a plasma membrane-bound enzyme, showed an increase in activity, whereas succinate dehydrogenase and Mn-Superoxide dismutase, both mitochondrial-bound enzymes, exhibited decreased activities. Lysosomal acid phosphatase displayed an increase in free activity and retention of latent activity inside the organelle. No alteration in free activity was shown by acid cathepsin. The cholinesterases did not exhibit any changes in activities nor did the cytosolic enzymes Cu/Zn-superoxide dismutase and lactate dehydrogenase. The decrease activity of the respiratory mitochondrial enzyme succinate dehydrogenase may contribute to the reduction in intraocular pressure, and the ability of the lysosomal organelles to retain their hydrolytic enzymes, ensures recovery of the cell from acute inflammatory attack.
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PMID:Enzymatic activities in the iris-ciliary body of the rabbit eye during experimentally induced acute ocular inflammation. 349 78

Cytochemistry was used to measure the activity of succinate dehydrogenase (SOD), lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G-6-PDH) in rat peritoneal macrophages under the action of the endogenous immunostimulant tuftcin (tre-lys-pro-arg) during phagocytosis of latex particles and at rest. Tuftcin did not affect the activity of the study enzymes in non-phagocytic cells. Elevation of the peptide concentration to 0.25 micrograms/ml and higher in phagocytic macrophages activated G-6-PDH and lowered the activity of LDH. Tuftcin did not alter the activity of SOD in phagocytic macrophages.
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PMID:[Effect of tuftsin on the activity of energy metabolism enzymes in peritoneal macrophages]. 398 36

Certain metalloproteins are common to all photosynthetic electron transfer chains. These include soluble proteins such as ferredoxins and cytochromes of the c2 type, and membrane-bound components such as cytochrome b, c1 and the Rieske iron-sulphur protein. The sequence of electron transfer Quinone leads to (cyt b, Fe-S, cyt c1) leads to cyt c2 indicates a common precursor to these systems and to the mitochondrial respiratory chain. In cyanobacteria the cytochrome c2 can be interchanged with the copper protein plastocyanin, and furthermore in chloroplasts of higher plants the latter is used exclusively. The ferredoxins in anaerobic photosynthetic bacteria are mostly of the [4Fe-4S] type, probably derived from those of the fermentative bacteria. These could readily be formed in the earliest cells from iron, sulphide and a very simple peptide. In the oxygen-evolving cyanobacteria and the aerobic halobacteria the [2Fe-2S] ferredoxins predominate. The electron transfer chains of the cyanobacteria have been incorporated almost unchanged into the chloroplasts of plants. The electron transfer chains of purple photosynthetic bacteria were probably the precursors of the mitochondrial respiratory chain, as shown by similarities of cytochromes c2 and succinate dehydrogenase. However a different origin of the eukaryotic cytoplasm is indicated by the presence of the copper/zinc superoxide dismutase.
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PMID:Metalloproteins in the evolution of photosynthesis. 727 71

The human TNF promoter contains four potential nuclear factor-kappa B (NF-kappa B)-binding sites, with the strongest binding seen for the -605 motif. Nuclear extracts from unstimulated cells of the human monocytic cell line, Mono Mac 6, contain one specific binding protein (complex II), consistent with a constitutive p50 homodimer. Stimulation of Mono Mac 6 cells with LPS will increase complex II and will strongly induce a second specific complex (complex I), which represents the p50/65 heterodimer. Treatment of Mono Mac 6 cells with pyrrolidine-dithiocarbamate (PDTC) at 300 microM will block the LPS-induced complex I almost completely and will reduce complex II to the constitutive level. Binding activity of other nuclear factors that recognize the SP-1 and c/EBP motifs of the human TNF promoter is not affected by such treatment. Northern blot analysis demonstrates that PDTC treatment will strongly reduce LPS-induced TNF transcripts. Secreted TNF protein as detected in the Wehi 164S/ActD bioassay and in a sandwich immunoassay was similarly reduced by PDTC. Kinetic analyses show that after LPS stimulation, NF-kappa B will peak at 1 h, TNF transcript prevalence at 2 h, and TNF protein at 4 h. PDTC did not shift this response to LPS to a later time, but suppressed NF-kappa B mobilization, TNF transcripts, and TNF protein over the entire 8-h observation period. Analysis of freshly isolated, LPS-stimulated blood monocytes showed a similar blockade of NF-kappa B. Furthermore, in these primary cells, induction of TNF transcripts, as determined by Northern blot analysis and by quantitative polymerase chain reaction, was prevented by PDTC as was TNF protein production. These data show that dithiocarbamates can profoundly affect cytokine expression and suggest that NF-kappa B is involved in LPS-induced TNF gene expression in human monocytes.
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PMID:Pyrrolidine dithiocarbamate inhibits NF-kappa B mobilization and TNF production in human monocytes. 825 5

To investigate the pathogenesis of retina lesions caused by intraocular pressure elevation, activities and distribution of enzymes in retina including lactic dehydrogenase (LDH), succinate dehydrogenase (SDH), adenosinetriphosphatase (AT-Pase), acid phosphatase (ACP), cholinesterase (ChE), cytochrome oxidase (CCO), nucleotidase (5'-Nase) and glucose-6-phosphatase (G6Pase) were determined histochemically in 30 rabbits. It was found that 1) in the early stage of intraocular pressure elevation, the activities of LDH, SDH, ATPase, ACP, and ChE in retina were increased, while the activities of CCO, 5'-Nase decreased; 2) in the late stage of intraocular pressure elevation, the activities of all these enzymes but ACP, which showed a reduced activity, were close to the normal level; 3) in superoxide dismutase.(SOD-CCE) treated group, except the slight increase of LDH and G6Pase activities, the activities of the remaining enzymes were near to normal. Our results suggest that the various histochemical changes in retina induced by intraocular pressure elevation were compensatory in the early stage and were beneficial to the supply of energy needed in retinal tissue and cellular metabolism; while in the late stage, the lesion of retina cells developed due to decompensation. SOD-CCE could alleviate the retinal lesions caused by intraocular pressure elevation, and can be used as auxiliary drug for the treatment of intraocular pressure elevation.
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PMID:Enzymatic histochemistry of retina with experimental intraocular pressure elevation in rabbits. 873 48

Yeast deficient in the cytosolic copper/zinc superoxide dismutase (SOD1) exhibit metabolic defects indicative of oxidative damage even under non-stress conditions. To help identify the endogenous sources of this oxidative damage, we isolated mutant strains of S. cerevisiae that suppressed metabolic defects associated with loss of SOD1. Six complementation groups were isolated and three of the corresponding genes have been identified. One sod1Delta suppressor represents SSQ1 which encodes a hsp70-type molecular chaperone found in the mitochondria. A second sod1Delta suppressor gene, designated JAC1, represents a new member of the 20-kDa J-protein family of co-chaperones. Jac1p contains a mitochondrial targeting consensus sequence and may serve as the partner for Ssq1p. Homologues of Ssq1p and Jac1p are found in bacteria in close association with genes proposed to be involved in iron-sulfur protein biosynthesis. The third suppressor gene identified was NFS1. Nfs1p is homologous to cysteine desulfurase enzymes that function in iron-sulfur cluster assembly and is also predicted to be mitochondrial. Each of the suppressor mutants identified exhibited diminished rates of respiratory oxygen consumption and was found to have reduced mitochondrial aconitase and succinate dehydrogenase activities. Taken together these results suggest a role for Ssq1p, Jac1p, and Nfs1p in assembly/maturation of mitochondrial iron-sulfur proteins and that one or more of the target Fe/S proteins contribute to oxidative damage in cells lacking copper/zinc SOD.
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PMID:Suppressors of superoxide dismutase (SOD1) deficiency in Saccharomyces cerevisiae. Identification of proteins predicted to mediate iron-sulfur cluster assembly. 981 17

These serial clinical and experimental studies were designed to clarify the pathogenesis of postburn MODS. Both animal and clinical studies were performed. In animal experiments, 46 male cross-bred dogs were cannulated with Swan-Ganz catheters and 39 of them were inflicted with 50% TBSA third degree burns (7 were used as controls). The burned dogs were randomly divided into 4 groups: immediate infusion, delayed infusion, delayed fast infusion and delayed fast infusion combined with ginsenosides. All dogs were kept under constant barbiturate sedation during the whole study period. Hemodynamics, visceral MDA, mitochondrial respiratory control rate (RCR) and ADP/O ratio, ATP, succinic dehydrogenase (SDH), organ water content as well as light and electron microscopy of visceral tissues were determined. In the clinical study, 61 patients with extensive deep burns were chosen, of which 16 sustained MODS. Plasma TXB2/6-keto-PGF1alpha ratio, TNF, SOD, MDA, circulatory platelet aggregate ratio (CPAR), PGE2, interleukin-1, total organ water content and pathological observations of visceral tissues from patients who died of MODS were carried out. Results demonstrated that ischemic-reperfusion damage due to severe shock, sepsis and inhalation injury are three main causes of postburn death. All inflammatory mediators increased markedly in both animals and patients who sustained organ damage or MODS. SDH, RCR, ADP/O and ATP decreased significantly. These findings suggested that ischemic damage and systemic inflammatory response syndrome (SIRS) initiated by mediators or cytokines might be important in the pathogenesis of postburn MODS.
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PMID:Serial experimental and clinical studies on the pathogenesis of multiple organ dysfunction syndrome (MODS) in severe burns. 991 70

We hypothesized that transient high-glucose concentration interferes with mediation by nitric oxide (NO) of flow-induced dilation (FID) of arterioles due to enhanced production of superoxide. In isolated, pressurized (80 mmHg) rat gracilis muscle arterioles ( approximately 130 microm) after transient high-glucose treatment (tHG; incubation with 30 mM glucose for 1 h), FID was reduced (maximum: control, 38 +/- 4%; after tHG, 17 +/- 3%), which was not further diminished by the NO synthase (NOS) inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME; 18 +/- 2%). Correspondingly, an enhanced polyethylene-glycol-SOD (PEG-SOD)-sensitive superoxide production was detected after tHG in carotid arteries by dihydroethydine (DHE) staining. Presence of PEG-SOD during tHG prevented the reduction of FID (41 +/- 3%), which could be inhibited by l-NAME (20 +/- 4%). Administration of PEG-SOD after tHG did not prevent the reduction of FID (22 +/- 3%). Sepiapterin, a precursor of the NO synthase cofactor tetrahydrobiopterin (BH(4)), administered during tHG did not prevent the reduction of FID (maximum, 15 +/- 5%); however, it restored FID when administered after tHG (32 +/- 4%). Furthermore, inhibition of either glycolysis by 2-deoxyglucose or mitochondrial complex II by 2-thenoyltrifluoroacetone reduced the tHG-induced DHE-detectable enhanced superoxide production in carotid arteries and prevented FID reduction in arterioles (39 +/- 5 and 35 +/- 2%). Collectively, these findings suggest that in skeletal muscle arterioles, a transient elevation of glucose via its increased metabolism, elicits enhanced production of superoxide, which decreases the bioavailability of NO and the level of the NOS cofactor BH(4), resulting in a reduction of FID mediated by NO.
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PMID:Microvascular dysfunction after transient high glucose is caused by superoxide-dependent reduction in the bioavailability of NO and BH(4). 1504 90

This study was designed to investigate the cardioprotective effects of preconditioning with 3-nitropropionic acid, an inhibitor of mitochondrial succinate dehydrogenase. 16 isolated rat hearts were randomly divided into two groups, a treatment group and a control group. The rats of the treatment group were treated intraperitoneally with 3-nitropropionic acid (3-NPA, 4 mg/kg) and the rats of the control group were treated with saline. 24 h after the treatment, the isolated hearts were mounted on a Langendorff apparatus. After 30 min, the hearts were subjected to 30-min ischemia and 60-min reperfusion. The HR, LVDP and +/- dp/dt(max) were measured at pre-ischemia and 30 min, 60 min after the reperfusion. Coronary effluent was collected 15 min after the reperfusion for the determination of CK and LDH. At the end of the 60-min reperfusion the heart was removed for the determination of myocardial SOD and MDA. Our results showed that in the 3-NPA group LVDP and +/- dp/dt(max) recovered significantly better, myocardial MDA, CK and LDH were significantly lower and the myocardial SOD was significantly higher than in the control group. It is concluded that chemical preconditioning by 3-nitropropionate has cardioprotective effects against ischemia-reperfusion injury.
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PMID:Chemical preconditioning by 3-nitropropionic acid reduces ischemia-reperfusion injury in rat heart. 1619 97

In this study the effects of stable and intermittent high glucose concentrations on ICAM-1, VCAM-1 and E-selectin production, PKC activity and PKCbetaI, betaII and delta isoforms expression in cultured HUVEC have been examined. In stable high glucose ICAM-1, VCAM-1 and E-selectin concentration and mRNA expression increased, and this effect was even more evident in intermittent high glucose. PKC activity increased in fluctuating glucose compared to stable high glucose, due to an over-expression of betaI, betaII and delta isoforms. ICAM-1, VCAM-1 and E-selectin, after the adding of total PKC inhibitor bisindolylmaleimide-I (BIMI-I) and LY379196, a specific inhibitor of PKCbeta, were equally reduced. 8-Hydroxydeoxyguanosine (8-OHdG), a sensitive indicator of oxidative damage to DNA, increased in stable and even more in intermittent high glucose and was reduced by both BIMI-I and LY379196. However, when thenoyltrifluoroacetone (TTFA), an inhibitor of mitochondrial complex II and the SOD mimetic Mn(III)tetrakis(4-benzoic acid) porphyrin chloride (MnTBAP) were added, all adhesion molecules, any PKC isoforms expression and 8-hydroxydeoxyguanosine were normalized in both constant and oscillating glucose. In conclusion intermittent high glucose induces a greater expression of the adhesion molecules than stable high glucose; this effect seems to be related to an activation of PKCbeta, but completely dependent from mitochondrial free radicals over-production.
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PMID:Intermittent high glucose enhances ICAM-1, VCAM-1 and E-selectin expression in human umbilical vein endothelial cells in culture: the distinct role of protein kinase C and mitochondrial superoxide production. 1628 92


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