Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
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Drug
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Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: EC:1.3.5.1 (
succinate dehydrogenase
)
8,177
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We have previously shown that acute coronary occlusion in the dog is often accompanied by increased adrenaline release into the blood. In the present study the consequences of this humoral reaction were studied in anaesthetised healthy mongrel dogs subjected to adrenaline infusion administered at a rate relevant to spontaneous release of this amine in coronary occlusion.
Adrenaline
was infused in a dose of 1.2 microgram.kg-1.min-1 for 4 h. Dogs receiving saline served as the control.
Adrenaline
administration led to the decrease in insulin/glucose ratio, to a significant fall in serum triiodothyronine and in blood pH. Free fatty acid levels doubled. Histochemically, a diminution in
succinic dehydrogenase
and ATPase activity in adrenaline-treated hearts was found. A significant fall in the activity of mitochondrial hexokinase in these hearts was detected spectrophotometrically. Electron microscopic study revealed alterations in the mitochondrial structure. These findings indicate that an excess of adrenaline in ammounts similar to that seen in experimental infarction leads to profound metabolic and hormonal disturbances and exerts a detrimental effect upon myocardium.
...
PMID:Evidence for the detrimental effect of adrenaline infused to healthy dogs in doses imitating spontaneous secretion after coronary occlusion. 2 14
Proteolytic activities in bovine adrenocortical mitochondria were investigated using [14C-methyl]casein as a substrate. Washed mitochondria showed a low proteolytic activity at pH 7.5 or 8.2. ATP (5 mM) plus MgCl2 (7.5 mM) stimulated the proteolysis 9 times at pH 8.2. It was further demonstrated unequivocally by various approaches that the ATP-dependent proteolytic activity localizes in mitochondrial matrix. The activity of the solubilized protease was sensitive to N-ethylmaleimide, mersalyl acid, phenylmethylsulfonyl fluoride, o-vanadate, m-vanadate, vanadyl sulfate, and quercetin but not by oligomycin and ouabain. The ATP-dependent proteolytic activity was eluted at the position of 650,000 daltons on an Ultrogel AcA 22 column as a single symmetrical peak. The gel-filtered enzyme showed high specificity to ATP. GTP and UTP partially substituted ATP. ADP, AMP, tripolyphosphate, alpha, beta-methylene ATP, and beta, gamma-methylene ATP had little or no stimulating activity. ATP did not stimulate the activity in the absence of MgCl2. We measured ATP-dependent proteolytic activities in mitochondrial fractions from several tissues in rat and bovine.
Adrenal
cortex was one of the tissues of highest activity. In addition, we investigated the effect of adrenal atrophy on the ATP-dependent protease activity in rat adrenal. The ATP-dependent protease activity/adrenal decreased by dexamethasone treatment. The extent of the decrease was similar to that of cytochrome oxidase and
succinate dehydrogenase
, but smaller than that of cytochrome P-450.
...
PMID:ATP-dependent protease in bovine adrenal cortex. Tissue specificity, subcellular localization, and partial characterization. 298 96
The effect of negative air ions (NAI) inhalation by rats on energy reactions of mitochondria in homogenates of liver and brain was studied. The influence of NAI was investigated under activation of animals by administration of physiological dose of adrenaline.
Adrenaline
administration induced hyperactivation of the rate of phosphorylating oxidation of succinic acid in liver and brain mitochondria which was accompanied by oxalacetate inhibition of
succinate dehydrogenase
(
SDH
) as well as excessive Ca2+ accumulation in liver mitochondria. These changes connected with a decrease of coefficient of phosphorylation efficiency ADP/O and uncoupler stimulation of respiration evidenced decrease of energy control of respiration in mitochondria. NAI inhalation diminished the rate of hyperactivated respiration and abolished excessive Ca2+ accumulation. These changes together with ADP/O coefficient and DNP stimulation increase evidence improvement of energy control of respiration which provide more moderate function of the respiratory chain under activation by adrenaline. Animals were excited by adrenaline administration. This effect was abolished by NAI inhalation, animals relaxed, some fell asleep. The data evidence sensitivity of mitochondrial processes in internal organs to inhalation of NAI and show participation of mitochondria in realization of physiological effects of NAI.
...
PMID:[Optimization of energy-dependent processes in mitochondria from rat liver and brain after inhalation of negative air ions]. 991 36
The laboratory workup of patients with pheochromocytoma and extra-adrenal paraganglioma (PPGLs) has traditionally focused on biochemical measurements of tumor secretory products or their metabolites, with ultimate diagnosis resting on routine histopathology and immunohistochemistry. While such testing remains important, the needs to distinguish potentially metastatic from benign tumors and to identify tumors with a hereditary basis have stimulated searches for additional means to stratify patients according to risk of metastasis or presence of a particular mutation. Biomarkers based on traditional biochemical tests, such as profiles of catecholamine metabolites and granin-derived peptides, provide utility for both purposes, while novel biomarkers are being identified by proteomic and transcriptomic studies, the latter including microRNA expression profiling. Histopathological scoring methods for predicting metastatic potential, such as the Pheochromocytoma of the
Adrenal
Gland Scaled Score (PASS), are limited by poor interobserver concordance, discrepant results between studies and incomplete knowledge of how scores relate to genotype. Immunohistochemical staining for
succinate dehydrogenase
(
SDH
) subunit B to triage patients for genetic testing of
SDH
subunit genes illustrates the growing importance of pathology as an adjunct to genetic testing for disease stratification. Although considerable effort has been expended on microarray-based platforms to identify biomarkers of malignancy, as yet, none of those proposed have been demonstrated to reliably discriminate malignant from benign disease any better than the PASS. Because of the heterogeneity of PPGLs and variable time between first appearance of tumors and identification of metastases, any prospective study to establish prognostic efficacy requires large numbers of patients and extended follow-up.
...
PMID:Diagnostic tests and biomarkers for pheochromocytoma and extra-adrenal paraganglioma: from routine laboratory methods to disease stratification. 2218 Feb 88
Pheochromocytomas are uncommon neuroendocrine tumors arising in the adrenal medulla, whereas paragangliomas arise from chromaffin cells in sympathetic and parasympathetic locations outside of the adrenal gland. Molecular genetic studies in the past few years have identified >10 genes involved in the pathogenesis of pheochromocytomas and paragangliomas, including RET oncogene, involved in the pathogenesis of multiple endocrine neoplasia (MEN) 2A and 2B, von Hippel-Lindau tumor-suppressor gene, neurofibromatosis type 1 gene,
succinate dehydrogenase
, THEM127, and several others. The presence of genetic alterations in some of these genes such as in MEN 2A and 2B can be used to diagnose these disorders clinically, and other mutations such as
succinate dehydrogenase
can be used in the pathologic prediction of benign and malignant pheochromocytomas and paragangliomas. Although it has been difficult to separate benign and malignant pheochromocytomas and paragangliomas, recent studies that may predict the behavior of these chromaffin-derived neoplasms have been reported. The Pheochromocytoma of the
Adrenal
Scale Score and the Grading system for Adrenal Pheochromocytoma and Paraganglioma scoring system are also discussed.
...
PMID:Pheochromocytomas and Paragangliomas: An Update on Recent Molecular Genetic Advances and Criteria for Malignancy. 2626 10