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)

Binding studies with (-)-[125I]cyanopindolol (ICYP) were conducted to characterize beta-adrenoceptors in plantaris and soleus muscles of rats (male, 250-300 g). The distribution of beta 1- and beta 2-adrenoceptors in different muscle fiber types, identified in serial sections by succinic dehydrogenase (SDH) staining, was studied by autoradiography. The densities of binding sites (Bmax, fmol/mg protein) were 5.4 +/- 0.9 (mean +/- SEM) in plantaris and 11.5 +/- 2.0 in soleus muscle. In plantaris muscle, monophasic competition curves were observed when binding experiments were performed using CGP20712A (50 pM to 0.5 mM), a beta 1-adrenoceptor selective antagonist, or ICI 118,551 (50 pM to 20 microM), a beta 2-adrenoceptor selective antagonist, to compete for ICYP binding. Analysis with LIGAND revealed a single binding site with a KD value of 2.41 +/- 0.56 nM (mean +/- SEM) for ICI 118,551 and 8.93 +/- 3.00 microM for CGP 20712A, indicating the presence of a homogeneous population of beta 2-adrenoceptors. In soleus muscle, competition curves were biphasic with 16-21% beta 1-adrenoceptors. Autoradiographic studies supported the findings from binding studies with membrane homogenates. The ICYP binding pattern was associated closely with the muscle fiber types identified by SDH staining. Propranolol-resistant binding sites were observed, and these sites were associated with muscle fibers positive to SDH staining.
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PMID:Characterization of beta 1- and beta 2-adrenoceptors in rat skeletal muscles. 168 10

Transforming growth factor-beta (TGF-beta) is a multifunctional growth factor that can either stimulate or inhibit cellular proliferation depending on cell type and culture conditions. The immunohistochemical localization of TGF-beta was investigated in human retinas and choroids using streptavidin peroxidase immunohistochemistry and a polyclonal rabbit antibody directed against the N-terminal 30 amino acids of TGF-beta 1. This antibody recognizes the beta 1 form of TGF-beta but not beta 2. TGF-beta localization was observed exclusively in photoreceptors in all adult non-diabetic and non-insulin dependent diabetic eyes, and 4 of 6 insulin dependent eyes. It was determined that TGF-beta was associated with both rods and cones using localization of peanut agglutinin (PNA), a lectin which binds to cone sheaths, on serial sections. Chondroitinase ABC digestion of sections prior to immunohistochemistry did not reduce TGF-beta immunoreactivity, suggesting that binding was not to glycosaminoglycans in the interphotoreceptor matrix. TGF-beta immunoreactivity was not observed in 2 premature human eyes in which photoreceptor outer segments had not yet developed. Localization in photoreceptors was also not observed in photocoagulation scars, in atrophic regions in a diabetic retina, nor in detached areas of retina from a young victim of head trauma. Based on PNA binding, succinate dehydrogenase enzyme histochemistry and phase contrast microscopy on adjacent sections, the TGF-beta negative areas of these retinas did not appear to have viable photoreceptors. This work demonstrates that TGF-beta is found exclusively in viable adult human retinal photoreceptors. It's function in these cells is currently not known.
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PMID:Immunohistochemical localization of transforming growth factor-beta in human photoreceptors. 202 49

The protective effects of beta 1-adrenergic blockade with metoprolol (Betaloc Astra) were demonstrated in the gerbil model of myocardial injury provoked by acute ischaemic brain lesions. The myocardial injury was reversible and lipid droplet accumulation was its most striking morphological feature. These droplets were easy to measure in EM photographs and their size was expressed as percentage of sarcoplasmic volume. The EM data of fat accumulation were compared in hearts of carotid-ligated animals with and without metoprolol pretreatment, and in animals with the carotid isolated only, at standard intervals 3-48 h after operation. While in carotid-ligated-only animals the average myocardial fat contents rose to a peak of 1.9% at 10 h, in metoprolol pretreated animals the amount of fat was always significantly lower and started to return earlier to basal values (peak at 6 h, 1.1%). In carotid-isolated-only animals, fat accumulation peaked at 6-10 h (1.1%) and returned quickly to normal levels (0.34 +/- 0.18%). This effective pharmacological blockade with metoprolol strongly supports the concept of catecholamine mediation between acute intracranial lesions and myocardial injury. The background and significance of myocardial fat accumulation is discussed. The EM morphometry of fat droplets appears to be a suitable tool for quantification of reversible myocardial damage most useful for experimental evaluation of cardioprotective measures. As changes in succinic dehydrogenase histochemistry (from 'myofibrillar' to 'granular' pattern) correlated with EM measured fat accumulation, the simplicity and speed of the SDH method recommends itself for fast orientation about presence of myocardial damage.
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PMID:Quantitative evaluation of myocardial injury induced by acute cerebral ischaemia and its prevention by beta 1-adrenergic blockade. An ultrastructural morphometry study. 260 13

beta-Amyloid cores contain considerable amounts of D-Ser and D-Asp residues in Alzheimer's disease. We investigated the cytotoxic effects of various synthetic beta-amyloids, including D-Ser-substituted derivatives, on primary cultured neurons and nonneuronal HeLa cells. beta 25-35, its D-Ser26-substituted derivative, and beta 1-40 in 10-100 nM specifically suppressed mitochondrial succinate dehydrogenase activity [MTT [3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide] reduction] in HeLa cells, which are dependent on ATP production mainly from glycolysis, but did not exert detectable cytotoxicity, assessed by dye exclusion test, NADH levels, and uptake of [3H]Leu and [3H]Tdr. The beta-amyloids, on the other hand, did exert neurodegenerative effects on rat hippocampal cultured neurons in which ATP is mostly synthesized by the mitochondrion. The activities of beta 25-35 and [D-Ser26] beta 25-35 are dependent on their having beta-structures and not random forms. Although beta 25-35 was degraded rapidly by proteinase(s) in brain extract or leucine aminopeptidase, [D-Ser26] beta 25-35 is fairly resistant. These results indicate that one of the primary targets of beta-amyloids is suppression of mitochondrial succinate dehydrogenase, and the vulnerability of the brain of beta-amyloids can be explained by its large dependence on mitochondrial energy production. Moreover, racemization of serine residues of beta-amyloids may be involved in neurodegeneration and formation of senile plaques through escaping from the degradation process by brain proteinases.
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PMID:Suppression of mitochondrial succinate dehydrogenase, a primary target of beta-amyloid, and its derivative racemized at Ser residue. 897 58