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)

The activity of acid phosphatase and some dehydrogenases in the peripheral blood lymphocytes was compared with the development of cell immunity, assessed by the macrophage migration inhibition test, during chemical carcinogenesis in Wistar rats. At the early stages of the carcinogenesis the changes of the enzymatic activities of succinic dehydrogenase and acid phosphatase proved to coordinate with a sufficiently high level of the immunological reactivity of the cell type in 66% of the animals. With the progressive growth of the tumours there occurred a disturbance of the enzymatic balance in the lymphoid cells and a simultaneous decrease in the immunological response.
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PMID:[Enzymatic and immunologic activity of lymphocytes during chemical carcinogenesis]. 82 Mar 86

The 78-kDa glucose-regulated protein (GRP78) is ubiquitously expressed in many cell types. Its promoter contains multiple protein-binding sites and functional elements. In this study we examined a high affinity protein-binding site spanning bp -198 to -180 of the rat grp78 promoter, using nuclear extracts from both B-lymphoid and HeLa cells. This region contains a sequence TGACGTGA which, with the exception of one base, is identical to the cAMP-response element (CRE). Site-directed mutagenesis reveals that this sequence functions as a major basal level regulatory element in hamster fibroblast cells and is also necessary to maintain high promoter activity under stress-induced conditions. By gel mobility shift analysis, we detect two specific protein complexes. The major specific complex I, while immunologically distinct from the 42-kDa CRE-binding protein (CREB), binds most strongly to the grp site, but also exhibits affinity for the CRE consensus sequence. As such, complex I may consist of other members of the CREB/activating transcription factor protein family. The minor specific complex II consists of CREB or a protein antigenically related to it. A nonspecific complex III consists of the Ku autoantigen, an abundant 70- to 80-kDa protein complex in HeLa nuclear extracts. By cotransfection experiments, we demonstrate that in F9 teratocarcinoma cells, the grp78 promoter can be transactivated by the phosphorylated CREB or when the CREB-transfected cells are treated with the calcium ionophore A23187. The differential regulation of the grp78 gene by cAMP in specific cell types and tissues is discussed.
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PMID:A binding site for the cyclic adenosine 3',5'-monophosphate-response element-binding protein as a regulatory element in the grp78 promoter. 183 91

It has been established that the concentration of nucleic acids, protein, glycogen, ATP, copper, manganese, zinc as well as the activity of cytochromoxidase and succinate dehydrogenase in tissues of the thymus gland and spleen of albino rats a day after stimulation by phytohemagglutinin increase considerably reaching the maximal values three days later. Taking a prolonged term (up to 7 days) after phytohemagglutinin administration it is found that the content and activity of the studied indices in the thymus and spleen tissues lower regularly, but fail reaching normal values even 14 days after stimulation. In this case changes in the test indices in the spleen are less pronounced than in the thymus in all the studied periods. In the tissues of adrenals a tendency of changes in the manganese and copper content is like that in lymphoid organs in all periods after stimulation by phytohemagglutinin; other test indices have an opposite tendency.
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PMID:[Stimulation of energy plastic metabolism by phytohemagglutinin in lymphoid organs and adrenal glands]. 255 46

Secondary lymphoid follicles in peripheral lymphoid organs (parathymic, mesenteric and inguinal lymph nodes and spleen) from young adult Wistar rats of both sexes were studied. Different numbers of tingible body macrophages containing aldehyde fuchsin-positive cytoplasmic granules of varying size, were present in the germinal centers. An identical staining pattern to that obtained with aldehyde fuchsin in terms of the number, distribution and size of positive cells was seen after staining for succinic dehydrogenase.
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PMID:Succinic dehydrogenase activity in germinal center macrophages in peripheral lymphoid organs of the rat. 288 60

The effect of rotaviruses and enterotoxigenic Escherichia coli administered in various sequences to cesarean-derived, colostrum-deprived calves was studied using light and electron microscopy. The structure of the lymphoid tissue in the ileum, the number of mitoses in the crypts, number of intraepithelial lymphocytes, and enzyme histochemistry (alkaline phosphatase, acid phosphatase, succinic dehydrogenase, beta-galactosidase, and leucinaminopeptidase) of the ileal dome epithelium were evaluated. The area of lymphoid follicles in Peyer's patches of the ileum was investigated morphometrically. Monoinfections with either rotavirus or enterotoxigenic E. coli induced a significant increase in lymphoid follicle area, but did not affect dome epithelial cells. Dual infections did not consistently affect the follicle area, but the number of intraepithelial lymphocytes and the mitotic indices exceeded those of comparable monoinfections. Changes in activity of enzymes in the ileal dome epithelial area were minor.
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PMID:Ileal Peyer's patches in experimental infections of calves with rotaviruses and enterotoxigenic Escherichia coli: a light and electron microscopic and enzyme histochemical study. 308 Aug 39

This study investigated changes in functional response to splenic T lymphocytes of mitogens following acute and chronic exposure to endurance exercise. Splenic T cell response in vitro to concanavalin A (Con A) and the total number of lymphocytes per spleen were compared between mice assigned to the following treatment conditions: (a) exercise training (EX) by treadmill running (28 m/min, 8 degrees slope for 30 min, 5 times per week for 4 weeks preceded by 2 weeks of endurance build-up), (b) exercise training as above followed by a single, acute bout of exercise to exhaustion (EX + AC) (35 m/min, 8 degrees slope, 30 min to 2 h duration) (c) exposure to the novel environment for 6 weeks without exercise (control), and exposure to the novel environment as in (c) followed by a single, acute bout of exercise to exhaustion. Treadmill running for 6 weeks significantly enhanced succinate dehydrogenase activity in skeletal muscle compared to the sedentary, control condition, and was broadly interpreted as indicative of a training effect. EX mice had significantly reduced splenic lymphocyte proliferative responses to optimal and supraoptimal concentrations of Con A compared with control animals. Incorporation of [3H]thymidine into splenic lymphocytes from EX + AC mice was the most markedly depressed. Total number of lymphocytes per spleen was significantly lower in EX compared with control mice. These results suggests that chronic exercise challenge in mice is associated with T lymphocyte hyporesponsiveness in the secondary lymphoid organs, such as the spleen.
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PMID:Chronic exercise stress in mice depresses splenic T lymphocyte mitogenesis in vitro. 349 54

Histochemical investigations were carried out to demonstrate the activity of succinic dehydrogenase, diphosphopyridine-nucleotid-diaphorase, alkaline phosphatase, and acid phosphatase in the liver, kidneys, lymph nodes, and heart muscle of a total of 20 cows with positive serologic response for leukosis as well as in organs of 2 normal controls. It was found that the lymphoid cells of the leukotic proliferations and the activated endothelial and adventitial cells of the blood vessels had high alkaline phosphatase activity and negligibly expressed acid phosphatase activity. Dehydrogenase activity was low in the lymphoid-cell proliferations and in the activated cell of the vessels. The cell metabolism of the leukotic proliferations was like-wise disturbed. Histochemical methods of investigations could be used test-like in the diagnosis of bovine leukosis.
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PMID:[Histochemical changes in leukemia in cattle]. 399 26

In an analysis of nitric oxide (.NO) production and toxicity, chicken macrophage-generated .NO inhibited mitochondrial activity in both .NO-producing macrophages themselves and lymphoid tumor targets. However, differences in targeting of mitochondrial toxicity were observed among these cells. Two chicken macrophage cell lines, HD11 and MQ-NCSU, produced .NO (measured as nitrite) dependent upon concentrations of L-arginine and bacterial endotoxin (lipopolysaccharide). Mitochondrial activity was negatively correlated with the amount of .NO produced. Using a modified MTT assay, .NO induced suppression in two mitochondrial complexes. Mitochondrial activity was significantly suppressed among HD11 cells receiving LPS alone (complex I, 63.0 +/- 5.5% suppression; complex II, 27.9 +/- 5.2%). In contrast, mitochondrial activities in samples receiving LPS plus inhibitor, NG-nitro-L-arginine methyl ester (NAME; 5 mM) or 2,4-diamino-6-hydroxypyrimidine (DAHP; 5 mM), were not significantly different from control values. When HD11 macrophages were cocultured with lymphoblastoid tumor targets, RECC-CU60 (T cell) or LSCC-RP9 (B cell), adding LPS (1 microgram/ml), tumor cell mitochondrial activity was significantly suppressed. In the generator macrophages, complex I was more suppressed than complex II, whereas in lymphoid targets no such difference was observed. These results indicate that .NO inhibits complex I and II mitochondrial activity but that differential targeting can occur among chicken leukocyte populations.
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PMID:Nitric oxide (.NO)-induced mitochondrial injury among chicken .NO-generating and target leukocytes. 802 70

Germline mutations in succinate dehydrogenase subunits B, C and D (SDHB, SDHC and SDHD), genes encoding subunits of mitochondrial complex II, cause hereditary paragangliomas and phaeochromocytomas. In SDHB (1p36)- and SDHC (1q21)-linked families, disease inheritance is autosomal dominant. In SDHD (11q23)-linked families, the disease phenotype is expressed only upon paternal transmission of the mutation, consistent with maternal imprinting. However, SDHD shows biallelic expression in brain, kidney and lymphoid tissues (Baysal et al., 2000). Moreover, consistent loss of the wild-type (wt) maternal allele in SDHD-linked tumours suggests expression of the maternal SDHD allele in normal paraganglia. Here we demonstrate exclusive loss of the entire maternal chromosome 11 in SDHD-linked paragangliomas and phaeochromocytomas, suggesting that combined loss of the wt SDHD allele and maternal 11p region is essential for tumorigenesis. We hypothesize that this is driven by selective loss of one or more imprinted genes in the 11p15 region. In paternally, but not in maternally derived SDHD mutation carriers, this can be achieved by a single event, that is, non-disjunctional loss of the maternal chromosome 11. Thus, the exclusive paternal transmission of the disease can be explained by a somatic genetic mechanism targeting both the SDHD gene on 11q23 and a paternally imprinted gene on 11p15.5, rather than imprinting of SDHD.
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PMID:Somatic loss of maternal chromosome 11 causes parent-of-origin-dependent inheritance in SDHD-linked paraganglioma and phaeochromocytoma families. 1506 8

The succinate dehydrogenase (SDH) complex exerts a fundamental role in mitochondrial cellular respiration and mutations in its encoding genes (SDHA, SDHB, SDHC, SDHD, collectively referred to as SDHx) lead to a number of inherited endocrine cancer predisposition syndromes, including familial paraganglioma/pheochromocytoma. Recent studies suggest a possible role for the SDH complex and other mitochondrial enzymes in the pathogenesis of hematological malignancy. Our aim was to search and identify pedigrees of patients affected by germline SHDx mutations treated at our institution for endocrine and other tumors, and seek to identify cases of hematological malignancy. We also analyzed cancer genome databases for reported cases of SDHx mutations outside of endocrine neoplasms. We report of two unrelated pedigrees carrying SDHx mutations with members affected by lymphomas. Sequencing data revealed one case of chronic lymphocytic leukemia with a SDHB mutation. This novel set of observations demonstrates the need for collaborative databases of patients with endocrine cancers with SDHx mutations, and the investigation of their role in hematological (lymphoid) malignancy.
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PMID:Exploring the association of succinate dehydrogenase complex mutations with lymphoid malignancies. 2478 45


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