Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male Wistar rats exposed to 50, 100 or 300 ppm methyl tertiary-butyl ether vapour for 2-15 weeks, 6 h daily, 5 days a week, showed a dose-dependent blood ether concentration after 2 weeks' exposure. Blood concentrations of tertiary-butanol, were also dose dependent indicating metabolic breakdown of the ether in vivo. The blood ether concentrations decreased after 6 weeks of exposure at the 50 ppm dose level and remained unaffected at higher doses while tertiary-butanol concentrations increased after 6 weeks with all doses, and began to decrease thereafter. Exposure caused a transient increase in UDP-glucuronosyltransferase activities in liver and kidney microsomes, almost no effects on hepatic cytochrome P-450 concentrations and a minor induction of kidney microsomal cytochrome P-450 content. Exposure produced almost no effect on brain succinate dehydrogenase, creatine kinase or acetylcholinesterase activities, while early inhibition of muscle creatine kinase activity was noted, accompanied by increased activity at the end of exposure.
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PMID:Biochemical effects of methyl tertiary-butyl ether in extended vapour exposure of rats. 409 53

Hydroxylamine chloride (0.3 g/l) in drinking water was given to 3-mo-old male Wistar rats for 1 to 63 days. The treatment caused splenomegalia while no effect was noted on the weight gain. Cerebral RNA content was also unaffected whereas slight decrease in the cerebral homogenate and isolated glial cell succinate dehydrogenase activities was found. Creatine kinase activity in the glial cell fractions increased after 63 days. An initial increase in the muscle acetylcholinesterase activity resolved in muscle after 2 wks while increased muscle creatine kinase activity was found throughout the experiment. The splenomegalia might have been caused by methemoglobinemic red cell fragility, an established NH2OH effect, while the neurochemical effects and effects on muscle might have resulted from direct toxicity rather than from the relative hypoxia because of impaired oxygen transport capacity.
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PMID:Neurochemical effects of ingested hydroxylamine. 608 90

Male Wistar rats exposed intermittently to 300 ppm (12.5 mumol/l) morpholine vapour 5 days a week for 6 h daily during 4-15 weeks displayed an increasing brain solvent content analyzed by a sensitive gas chromatographic method. Rats drinking water which contained 150 mg NaNO2/l during the vapour exposure period showed initially larger brain solvent concentrations which began to decrease after 8 weeks. Fat solvent concentrations were a fraction of those detected in brain of the solvent-exposed animals or of those in the combined exposure. Nitrite exposure alone caused decreased spinal cord axon acetylcholine esterase activity after 8 weeks while this effect was noted in the combined exposure only at 8 weeks disappearing later on. Axonal succinate dehydrogenase activity was below the controls in the combined exposure throughout the study, and combination also caused persistent increase in the muscle creatine kinase activity. The morpholine-induced effects were less remarkable. The results point at pharmacokinetic interaction between the solvent and nitrite with its own effects on energy metabolism. No N-nitrosomorpholine was found although other metabolic interactions could not be excluded.
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PMID:Morpholine vapour inhalation and interactions of simultaneous nitrite intake. Biochemical effects on rat spinal cord axons and skeletal muscle. 634 82

There is no effective treatment for the cardiomyopathy of the most common autosomal recessive ataxia, Friedreich's ataxia (FA). The identification of potentially toxic mitochondrial (MIT) iron (Fe) deposits in FA suggests that Fe plays a role in its pathogenesis. This study used the muscle creatine kinase conditional frataxin (Fxn) knockout (mutant) mouse model that reproduces the classical traits associated with cardiomyopathy in FA. We examined the mechanisms responsible for the increased cardiac MIT Fe loading in mutants. Moreover, we explored the effect of Fe chelation on the pathogenesis of the cardiomyopathy. Our investigation showed that increased MIT Fe in the myocardium of mutants was due to marked transferrin Fe uptake, which was the result of enhanced transferrin receptor 1 expression. In contrast to the mitochondrion, cytosolic ferritin expression and the proportion of cytosolic Fe were decreased in mutant mice, indicating cytosolic Fe deprivation and markedly increased MIT Fe targeting. These studies demonstrated that loss of Fxn alters cardiac Fe metabolism due to pronounced changes in Fe trafficking away from the cytosol to the mitochondrion. Further work showed that combining the MIT-permeable ligand pyridoxal isonicotinoyl hydrazone with the hydrophilic chelator desferrioxamine prevented cardiac Fe loading and limited cardiac hypertrophy in mutants but did not lead to overt cardiac Fe depletion or toxicity. Fe chelation did not prevent decreased succinate dehydrogenase expression in the mutants or loss of cardiac function. In summary, we show that loss of Fxn markedly alters cellular Fe trafficking and that Fe chelation limits myocardial hypertrophy in the mutant.
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PMID:The MCK mouse heart model of Friedreich's ataxia: Alterations in iron-regulated proteins and cardiac hypertrophy are limited by iron chelation. 1862 80

No previous study has used proteomics to investigate the effects of exercise training on human skeletal muscle. Five recreationally active men completed a 6-wk training programme involving three sessions per week, utilising six 1-min bouts at maximum oxygen uptake (V O(2)max) interspersed with 4 min at 50% V O(2)max. Vastus lateralis was biopsied at standardised times before and after the training intervention. Protein expression profiling was performed using differential analysis of 2-DE gels; complemented with quantitative analysis (iTRAQ) of tryptic peptides from 1-DE gel lane-segments using LC-MALDI MS/MS. Interval training increased average V O(2)max (7%; p<0.001) and was associated with greater expression of mitochondrial components, including succinate dehydrogenase, trifunctional protein-alpha and ATP synthase alpha- and beta-chains. 2-DE resolved 256 spots, and paired t-tests identified 20 significant differences in expression (false discovery rate <10%). Each differentially expressed gene product was present as multiple isoelectric species. Therefore, the differences in spot expression represent changes in post-transcriptional or post-translational processing. In particular, modulation of muscle creatine kinase and troponin T were prominent. Pro-Q Diamond staining revealed these changes in expression were associated with phosphorylated protein species, which provides novel information regarding muscle adaptation to interval training.
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PMID:Proteomic investigation of changes in human vastus lateralis muscle in response to interval-exercise training. 1983 92