Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.1.8 (acyl-CoA dehydrogenase)
 785 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic indirect stimulation (10 Hz) was performed on rabbit tibialis anterior muscle. Long-term stimulation (52-140 days) produced a transformation of the fast tibialis anterior into a slow red muscle as judged from the histochemistry of myofibrillar actomyosin ATPase, the pattern of myosin light chains and the thorough rearrangement of the enzyme activity pattern of energy metabolism. Activity levels of citrate synthetase (CS), malate dehydrogenase (MDH), succinate dehydrogenase (SDH), 3-hydroxy-acyl-CoA dehydrogenase (HAD), and lactate dehydrogenase (LDH) were determined quantitatively by either microbiochemical assays (CS, MDH, HAD and LDH) on microdissected, single fibres or by kinetic microphotometry on cross-sectioned fibres (SDH). The activity profiles of these enzymes displayed pronounced scattering in the fibre population of the unstimulated muscle. Despite a several fold increase in the activities of CS, MDH, SDH and HAD and a pronounced decrease in LDH, chronic stimulation failed to abolish the metabolic heterogeneity of the fibre population. It is possible that chronic indirect stimulation cannot produce uniformity of fibres because of continuing diverse natural activity of the motor units.
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PMID:Effects of chronic stimulation on the metabolic heterogeneity of the fibre population in rabbit tibialis anterior muscle. 674 46

To examine the effects of unweighting on the structural and metabolic adaptations of a non-postural muscle, deltoideus muscle biopsies were taken in seven male healthy subjects, before and after a 37 day bedrest. Myofibrillar ATPase histochemistry demonstrated no change in fibre type distributions (I, IIA, IIB), in fibre cross-sectional areas nor in capillary supply. No difference was noted in enzyme activities of oxidative metabolism (citrate synthase, 3-hydroxy-acyl-CoA dehydrogenase), and glycolysis (hexokinase, lactate dehydrogenase). Electron microscopy showed a decrease in the volume density of lipids but no change in mitochondrial volume density and distribution. The results indicate that bedrest induces no major morphological and biochemical changes in deltoideus muscle, contrary to what was previously reported in vastus lateralis muscle. This lack of changes is probably related to an unaltered deltoideus muscle use.
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PMID:Effects of bedrest on deltoideus muscle morphology and enzymes. 955 Feb 25

Ethylmalonic acid (EMA) accumulation occurs in various metabolic diseases with neurological manifestation, including short acyl-CoA dehydrogenase deficiency (SCADD) and ethylmalonic encephalopathy (EE). Since pathophysiological mechanisms responsible for brain damage in these disorders are still poorly understood, we investigated the ex vivo effects of acute intrastriatal administration of EMA on important parameters of energy and redox homeostasis in striatum from young rats. We evaluated CO(2) production from glucose, glucose utilization and lactate production, as well as the activities of the citric acid cycle (CAC) enzymes, the electron transfer chain (ETC) complexes II-IV (oxidative phosphorylation, OXPHOS) and synaptic Na(+),K(+)-ATPase. We also tested the effect of EMA on malondialdehyde (MDA) levels (marker of lipid oxidation) and reduced glutathione (GSH) levels. EMA significantly reduced CO(2) production, increased glucose utilization and lactate production, and reduced the activities of citrate synthase and of complexes II and II-III of the ETC, suggesting an impairment of CAC and OXPHOS. EMA injection also reduced Na(+),K(+)-ATPase activity and GSH concentrations, whereas MDA levels were increased. Furthermore, EMA-induced diminution of Na(+),K(+)-ATPase activity and reduction of GSH levels were prevented, respectively, by the antioxidants melatonin and N-acetylcysteine, indicating that reactive species were involved in these effects. Considering the importance of CAC and ETC for energy production and Na(+),K(+)-ATPase for the maintenance of the cell membrane potential, the present data indicate that EMA compromises mitochondrial homeostasis and neurotransmission in striatum. We presume that these pathomechanisms may be involved to a certain extent in the neurological damage found in patients affected by SCADD and EE.
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PMID:Disturbance of energy and redox homeostasis and reduction of Na+,K+-ATPase activity provoked by in vivo intracerebral administration of ethylmalonic acid to young rats. 2558 15