Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.3.99.3 (acyl-CoA dehydrogenase)
 1,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of erucic acid on the oxidative metabolism of rat-heart mitochondria have been investigated using intact animals, perfused beating heart, isolated mitochondria and mitochondrial extracts. Feeding rats with a diet containing erucic acid was found to lead to a diminished ability of the isolated heart mitochondria to oxidize various substrates, in accordance with previous reports (Houtsmuller et al., Biochim. Biophys. Acta 218 (1970) 564). This effect was almost pronounced with palmitylcarnitine as substrate, in which case the rate of oxidation was decreased by more than 50% at such a low erucic acid content in the diet as 1.4% given over 2-4 weeks. Oxidation of palmitylcarnitine was also found to be inhibited when erucylcarnitine was added to isolated heart mitochondria from control animals, in agreement with earlier observations (Christophersen and Bremer, FEBS Lett. 23 (1972) 230; Biochim. Biophys. Acta 280 (1972) 506). The inhibition was accompanied by a decrease in the rate and extent of reduction of mitochondrial flavoprotein. Experiments with perfused beating rat-heart likewise revealed an inhibition of flavoprotein reduction, as well as nicotinamide nucleotide reduction, when erucate was added to the perfusing medium of the beating heart respiring with oleate--but not with octanoate--as substrate. These data together with those earlier published in the literature indicate that erucic acid may interfere with the enzyme system involved in the mitochondrial oxidation of long-chain fatty acids, probably at the level of acyl-CoA dehydrogenase. Kinetic data supporting this conclusion, obtained with extracts of rat-heart mitochondria containing the acyl-CoA dehydrogenase and electron-transferring flavoprotein system, are presented. The possible implications of these results for the known effect of dietary erucic acid in causing an accumulation of fat in the heart are discussed.
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PMID:Studies of the mode of action of erucic acid on heart metabolism. 106 21

Muscle biopsy samples were collected from the middle gluteal muscle of seven horses undergoing a nine-month endurance training programme. Samples were collected before the programme began and again after three, six and nine months of training. A fifth sample was collected three months after training ceased. Serial muscle sections were reacted histochemically for myosin adenosine triphosphatase after either acid (pH 4.3 and 4.6) or alkaline (pH 10.3) pre-incubation, and muscle fibres identified as type I, IIA, IIB or IIC. The oxidative capacity of individual fibres was assessed, using the reduced nicotinamide dinucleotide tetrazolium reductase stain, and the number of intermyofibrillar capillaries adjacent to each fibre was counted after staining, using the alpha-amylase periodic acid Schiff technique. Biochemical analyses involved the fluorometric measurement of the enzymes citrate synthase, 3-hydroxy acyl CoA dehydrogenase and lactate dehydrogenase as markers of end terminal oxidative, beta oxidative and glycolytic potential, respectively. There was an increase in the percentage of type IIB fibres having high nicotinamide dinucleotide tetrazolium reductase staining after three months training. This increase persisted throughout the period of training and during the period without training. There was an increase in the number of capillaries adjacent to type IIB fibres after six and nine months training. These had returned to near pre-training numbers after three months without training. There were increases in the activities of citrate synthase and 3-hydroxy acyl CoA dehydrogenase after three months training. The activities of both enzymes continued to rise throughout training and the highest activities were attained after nine months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of a nine-month endurance training programme on muscle composition in the horse. 367 37

Biopsy samples were obtained from the middle gluteal muscle of 10 Thoroughbred horses undergoing a commercial race-training program. Samples were obtained before the program began and again after 6 and 12 weeks of training. All horses had raced at least once by the 12th week of training. Serial sections of muscle were examined histochemically for myosin adenosinetriphosphatase after either acid (pH 4.3 and 4.6) or alkaline (pH 10.3) preincubation, and then muscle fibers were identified as types I, IIA, IIB, or IIC. The oxidative capacity of individual fibers was assessed, using the reduced nicotinamide dinucleotide tetrazolium-reductase stain, and the number of intermyofibrillar capillaries adjacent to each fiber were counted after staining, using the alpha-amylase-periodic acid-Schiff technique. Biochemical analyses involved the fluorometric measurement of 3 enzymes--citrate synthase, 3-hydroxy-acyl coenzyme A dehydrogenase, and lactate dehydrogenase--as markers of end terminal oxidative, beta-oxidative, and glycolytic potentials, respectively. Changes in fiber-type percentages did not occur in response to training. There was a significant (P less than 0.01) increase in the percentage of type IIB fibers, having high nicotinamide dinucleotide-tetrazolium reductase staining after 12 weeks of training. Alterations in the number of capillaries adjacent to each fiber type did not occur during the training period. There were increases in the activities of both citrate synthase and 3-hydroxy-acyl coenzyme A dehydrogenase after 6 weeks (P less than 0.05) and 12 weeks (P less than 0.001) of training. Alterations in the activity of lactate dehydrogenase did not occur in response to training.
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PMID:Effects of training on muscle composition in horses. 394 89

Muscle biopsy specimens from the middle gluteal muscle were studied in 16 red blood cell hypervolaemic (Group HV) and 19 normovolaemic (Group NV) Standardbred racehorses. All horses were stallions, 4-8 years old and having similar mean racing performance values, as described by an individual selection index value. All horses raced regularly but those in Group HV did not perform as expected and were therefore referred to the clinics for exercise tolerance testing. Muscle biopsy specimens were analysed for fibre type distribution (Type I, IIA and IIB), fibre area and relative fibre area. In addition, oxidative capacity of the fibres was evaluated by staining for nicotinamide adenine dinucleotide (NADH) tetrazolium reductase, and the activities of citrate synthase, 3-OH-acyl CoA dehydrogenase and lactate dehydrogenase were analysed in whole-muscle samples. With the exception of a higher percentage of Type IIB fibres in Group HV having a high oxidative capacity as evaluated by the NADH stain, no significant difference were found in fibre composition, fibre area or enzyme activity between the Groups HV and NV.
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PMID:Skeletal muscle characteristics in red blood cell normovolaemic and hypervolaemic standardbred racehorses. 857