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succinate dehydrogenase/nekróza
Odkaz je uložen do schránky
Strana 1 z 119 Výsledek
Tumor necrosis factor induces activation of mitochondrial succinate dehydrogenase.
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Přihlášení Registrace
We have studied TNF-induced changes in mitochondrial enzymes. One enzyme, succinate dehydrogenase (SDH), is specifically activated in TNF sensitive cells including U937 (human monocytic), WEHI-164 (murine fibrosarcoma), and ME-180 (human cervical carcinoma). SDH is activated by TNF concentrations
Mechanisms of cell death induced by the mitochondrial toxin 3-nitropropionic acid: acute excitotoxic necrosis and delayed apoptosis.
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Impaired energy metabolism may play an important role in neuronal cell death after brain ischemia and in late-onset neurodegenerative diseases. Both excitotoxic necrosis and apoptosis have been implicated in cell death induced by metabolic impairment. However, the factors that determine whether
Alterations of Antioxidant Status and Mitochondrial Succinate Dehydrogenase Activity in the Liver of Wistar Strain Albino Rats Treated with by Ethanol Extracts of Annona senegalensis Pers (Annonaceae) Stem Bark.
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Numerous ethnomedicinal uses have been attributed to different parts of Annona senegalensis (ASE), including its uses as food and food additives. The present study investigated toxicological and antioxidant effects of 28 days administration of ethanol extracts of ASE stem bark to Wistar
Tumour necrosis factor-alpha induces superoxide anion generation in mitochondria of L929 cells.
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Within a few minutes after addition to L929 cells, tumour necrosis factor-alpha (TNF alpha) induced an increase in lucigenin-enhanced chemiluminescence that could be inhibited by superoxide dismutase. The generation of superoxide anion (O2.-) was sensitive to treatment with rotenone, antimycin A and
[Effects of bFGF on succinate dehydrogenase level and oxygen consumption of skin flap in rats].
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To investigate the effects of basic fibroblast growth factor (bFGF) on necrosis rate, succinate dehydrogenase level and oxygen consumption of the skin flap, 18 Wistar rats were divided into 2 groups. Caudally based skin flap was raised on the back of each rat. Nine micrograms bFGF or normal saline
Diglycolic acid inhibits succinate dehydrogenase activity in human proximal tubule cells leading to mitochondrial dysfunction and cell death.
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Diethylene glycol (DEG) is a solvent used in consumer products allowing the increased risk for consumer exposure. DEG metabolism produces two primary metabolites, 2-hydroxyethoxyacetic acid (2-HEAA) and diglycolic acid (DGA). DGA has been shown to be the toxic metabolite responsible for the proximal
The differential JunB responses to inhibition of succinate dehydrogenase in rat hippocampus and liver.
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The inhibitor of mitochondrial enzyme succinate dehydrogenase, 3-nitropropionic acid (3-NPA), induces cellular energy deficit followed by oxidative stress, secondary excitotoxicity and neuronal degeneration. The fast activation of Jun and Fos proteins and other proteins encoding inducible
MDCT features of succinate dehydrogenase (SDH)-deficient gastrointestinal stromal tumours.
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OBJECTIVE
To describe the multidetector CT (MDCT) features and metastatic pattern of succinate dehydrogenase (SDH)-deficient gastrointestinal stromal tumours (GISTs).
METHODS
In this institutional review board-approved, Health Insurance Portability and Accountability Act-compliant study, we
Death mode-dependent reduction in succinate dehydrogenase activity in hair cells of aging rat cochleae.
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BACKGROUND
Our previous studies have shown that both apoptosis and necrosis are involved in hair cell (HC) pathogenesis in aging cochleae. To better understand the biological mechanisms responsible for the regulation of HC death, we examined the activity of succinate dehydrogenase (SDH), a
Exeriences with isoprenaline induced myocardial necrosis in the rat.
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An attempt has been made to quantify myocardial lesions produced in the rat by isoprenaline for use as a model to assess possible incremental effects of environmental and dietary factors. This was initially made difficult by variation in the cardiotoxicity of different samples of isoprenaline.
Clinicopathologic features of succinate dehydrogenase deficiencient renal cell carcinoma
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According to the WHO new renal tumor classification (2016), the clinical and pathologic characteristics, immunophenotype and molecular genetic characteristics of 2 cases of succinate dehydrogenase (SDH)-deficient renal cell carcinoma were retrospectively analyzed, and the relevant literature was
Hepatic mitochondrial enzyme activity and serum amino acid composition in rats treated with tumor necrosis factor.
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The biochemical integrity of hepatocellular mitochondria was investigated in rats treated with small doses of human recombinant tumor necrosis factor-alpha (Hur-TNF;50-100 micrograms/kg/d injected intraperitoneally for 5 d) by measuring the activities of three mitochondrial enzymes, glutamate
Increased activity and sensitivity of mitochondrial respiratory enzymes to tumor necrosis factor alpha-mediated inhibition is associated with increased cytotoxicity in drug-resistant leukemic cell lines.
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The drug-resistant leukemic cell lines, CEM/VLB100 and K/DAU600, are more sensitive to tumor necrosis factor alpha (TNFalpha)-mediated cytotoxicity compared with their parental cell lines, CCRF-CEM and K562 cl.6. Drug-resistant leukemic cell lines have more active mitochondrial function, which is
Thiamine deficiency--induced partial necrosis and mitochondrial uncoupling in neuroblastoma cells are rapidly reversed by addition of thiamine.
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Culture of neuroblastoma cells in a medium of low-thiamine concentration (6 nM) and in the presence of the transport inhibitor amprolium leads to the appearance of overt signs of necrosis; i.e., the chromatin condenses in dark patches, the oxygen consumption decreases, mitochondria are uncoupled,
Mitigation of mitochondrial dysfunction and regulation of eNOS expression during experimental myocardial necrosis by alpha-mangostin, a xanthonic derivative from Garcinia mangostana.
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Oxidative stress can play a key role in myocardial necrosis. The present study was designed to investigate the effect of alpha-mangostin (an antioxidant phytonutrient) on mitochondrial dysfunction and endothelial nitric oxide synthase (eNOS) expression during isoproterenol-induced myocardial
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