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:2.3.3.1 (citrate synthase)
4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The capacity of white adipose tissue mitochondria to support a high beta-oxidative flux was investigated by comparison to liver mitochondria. Based on marker enzyme activities and electron microscopy, the relative purity of the isolated mitochondria was similar thus allowing a direct comparison on a protein basis. The results confirm the comparable capacity of adipose tissue and liver mitochondria for palmitoyl-carnitine oxidation. Relative to liver, both citrate synthase and alpha-ketoglutarate dehydrogenase were increased 7.87- and 10.38-fold, respectively. In contrast, adipose tissue NAD-isocitrate dehydrogenase was decreased (2.85-fold). Such modifications in the citric acid cycle are expected to severely restrict citrate oxidation in porcine adipose tissue. Except for cytochrome c oxidase, activities of the enzyme complexes comprising the electron transport chain were not significantly different. The decrease in adipose cytochrome c oxidase activity could partly be attributed to a decreased inner membrane as suggested by lipid and enzyme analysis. In addition, Western blotting indicated that adipose and liver mitochondria possess similar quantities of cytochrome c oxidase protein. Taken together these results indicate that not only is the white adipose tissue protoplasm relatively rich in mitochondria, but that these mitochondria contain comparable enzymatic machinery to support a relatively high beta-oxidative rate.
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PMID:Biochemical properties of porcine white adipose tissue mitochondria and relevance to fatty acid oxidation. 1143 34

The relationships between in vivo (31)P magnetic resonance spectroscopy (MRS) and in vitro markers of oxidative capacity (mitochondrial function) were determined in 27 women with varying levels of physical fitness. Following 90-s isometric plantar flexion exercises, calf muscle mitochondrial function was determined from the phosphocreatine (PCr) recovery time constant, the adenosine diphosphate (ADP) recovery time constant, the rate of change of PCr during the initial 14 s of recovery, and the apparent maximum rate of oxidative adenosine triphosphate (ATP) synthesis (Q(max)). Muscle fiber type distribution (I, IIa, IIx), citrate synthase (CS) activity, and cytochrome c oxidase (COX) activity were determined from a biopsy sample of lateral gastrocnemius. MRS markers of mitochondrial function correlated moderately (P < 0.05) with the percentage of type IIa oxidative fibers (r = 0.41 to 0.66) and CS activity (r = 0.48 to 0.64), but only weakly with COX activity (r = 0.03 to 0.26, P > 0.05). These results support the use of MRS to determine mitochondrial function in vivo.
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PMID:Relation between in vivo and in vitro measurements of skeletal muscle oxidative metabolism. 1174 76

To gain better insight into the insulin secretory activity of fetal beta cells in response to glucose, the expression of glucose transporter 2 (GLUT-2), glucokinase and mitochondrial glycerol phosphate dehydrogenase (mGDH) were studied. Expression of GLUT-2 mRNA and protein in pancreatic islets and liver was significantly lower in fetal and suckling rats than in adult rats. The glucokinase content of fetal islets was significantly higher than of suckling and adult rats, and in liver the enzyme appeared for the first time on about day 20 of extrauterine life. The highest content of hexokinase I was found in fetal islets, after which it decreased progressively to the adult values. Glucokinase mRNA was abundantly expressed in the islets of all the experimental groups, whereas in liver it was only present in adults and 20-day-old suckling rats. In fetal islets, GLUT-2 and glucokinase protein and their mRNA increased as a function of increasing glucose concentration, whereas reduced mitochondrial citrate synthase, succinate dehydrogenase and cytochrome c oxidase activities and mGDH expression were observed. These findings, together with those reported by others, may help to explain the decreased insulin secretory activity of fetal beta cells in response to glucose.
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PMID:Expression of glucose transporter-2, glucokinase and mitochondrial glycerolphosphate dehydrogenase in pancreatic islets during rat ontogenesis. 1178 5

In this study, we examined whether weight loss-induced changes in plasma organochlorine compounds (OC) were associated with those in skeletal muscle markers of glycolytic and oxidative metabolism. Vastus lateralis skeletal muscle enzyme activities and plasma OC (Aroclor 1260, polychlorinated biphenyl 153, p,p'-DDE, beta-hexachlorocyclohexane, and hexachlorobenzene) were measured before and after a weight loss program in 17 men and 20 women. Both sexes showed a similar reduction in body weight (approximately 11 kg) in response to treatment, although men lost significantly more fat mass than women (P < 0.05). Enzymatic markers of glycolysis, phosphofructokinase (PFK) activity, and oxidative metabolism, beta-hydroxyacyl-CoA dehydrogenase (HADH), citrate synthase (CS), and cytochrome c oxidase (COX) activities, remained unchanged after weight loss. A significant increase in plasma OC levels was observed in response to weight loss, an effect that was more pronounced in men. No relationship was observed between changes in OC and those in PFK activity in either sex [-0.31 < r < 0.12, not significant (NS)]. However, the greater the increase in plasma OC levels, the greater the reduction in oxidative enzyme (HADH, CS, COX) activities was in response to weight loss in men (-0.75 < r < -0.50, P < 0.05) but not in women (-0.33 < r < 0.33, NS). These results suggest that the weight loss-induced increase in plasma pollutant levels is likely to be associated with reduced skeletal muscle oxidative metabolism in men but not in women.
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PMID:Weight loss-induced rise in plasma pollutant is associated with reduced skeletal muscle oxidative capacity. 1183 59

We compared responses of the fast extensor digitorum longus (EDL) and tibialis anterior (TA) muscles in young (15-week) and aging (101-week) male Brown Norwegian rats to 50 days of chronic low-frequency stimulation (CLFS, 10 Hz, 10 hours/day). After 50 days of CLFS, the EDL muscles of the young (22-week) and aging (108-week) rats displayed similar increases in type IIA fibers, relative concentration of myosin heavy chain MHCIIa, elevations in mitochondrial citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities, and similar decreases in glycolytic enzyme activities (glyceraldehydephosphate dehydrogenase, lactate dehydrogenase). TA muscle in young rats contained a few cytochrome c oxidase negative (COX-) type I fibers. Their number was approximately 2-fold elevated by CLFS. Conversely, aging muscle, which contained a slightly higher amount of COX- fibers than young TA muscle, responded to CLFS with a significant decrease in COX- fibers. The appearance of small COX-positive type I fibers in stimulated aging muscle indicated that regenerating type I fibers "diluted" the COX-deficient fiber population.
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PMID:Adaptive potentials of skeletal muscle in young and aging rats. 1191 26

Mitochondria in cells isolated from the hepatopancreas of aestivating land snails (Helix aspersa) consume oxygen at 30% of the active control rate. The aim of this study was to investigate whether the lower respiration rate is caused by a decrease in the density of mitochondria or by intrinsic changes in the mitochondria. Mitochondria occupied 2% of cellular volume, and the mitochondrial inner membrane surface density was 17 microm(-1), in cells from active snails. These values were not different in cells from aestivating snails. The mitochondrial protein and mitochondrial phospholipid contents of cells were also similar. There was little difference in the phospholipid fatty acyl composition of mitochondria isolated from metabolically depressed or active snails, except for arachidonic acid, which was 18% higher in mitochondria from aestivating snails. However, the activities of citrate synthase and cytochrome c oxidase in mitochondria isolated from aestivating snails were 68% and 63% of control, respectively. Thus the lower mitochondrial respiration rate in hepatopancreas cells from aestivating snails was not caused by differences in mitochondrial volume or surface density but was associated with intrinsic changes in the mitochondria.
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PMID:Structure and function of mitochondria in hepatopancreas cells from metabolically depressed snails. 1202 89

The Swan River Estuary is the recipient of multiple urban and agricultural contaminants which have the potential to induce liver detoxication enzymes as well as altering the metabolism of aquatic organisms. To test if altered liver metabolism would influence liver detoxication capacities, pink snapper (Pagrus auratus) were i.p. injected with peanut oil (controls), or pentachlorobiphenyl #126 (PCB126), with sodium pentachlorophenate (NaPCP), or PCB126+NaPCP. Relative to controls, ethoxyresorufin-O-deethylase (EROD) activity was induced in the PCB126 and PCB126+NaPCP fish, but not in the NaPCP group. In the liver, cytochrome c oxidase (CCO) activity was enhanced by the treatments while citrate synthase (CS) activity remained unchanged and lactate dehydrogenase (LDH) activity was increased in the NaPCP treatment only. The results suggest that liver CCO activity may be a suitable biomarker of effect following exposure to PCBs or phenolic compounds. In the white muscle, only the PCB126+NaPCP treatment enhanced CCO activity, with all other enzymatic activities remaining unchanged. It appears that the resilience to metabolic perturbations is greater for white muscle than for liver. Low serum sorbitol dehydrogenase (sSDH) activity and histopathology of the liver indicated no significant alteration of cellular structure, albeit the lipid droplet size was increased in the PCB126 and in the PCB126+NaPCP treatments. It is concluded that the hepatic metabolic changes correspond to histopathological observations, but an altered metabolic capacity do not influence the metabolism of xenobiotics by liver enzymes, as measured by EROD activity.
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PMID:Metabolic disturbances in fish exposed to sodium pentachlorophenate (NaPCP) and 3,3',4,4',5-pentachlorobiphenyl (PCB126), individually or combined. 1222 98

Independent of apoptosis, dexamethasone induced and a decrease of respiration and citrate synthase activity per cell in cells with and without transgenic Bcl-2 expression. The reduction of respiration, however, was slightly, but statistically more pronounced in apoptotic cells compared to non-apoptotic Bcl-2 over-expressing cells. A slight cytochrome c release was detected in apoptotic cells only. Importantly, the stimulatory effect of FCCP was maintained, indicating that oxidative phosphorylation remained coupled in active mitochondria. Coupled and uncoupled respiration were reduced to almost identical degrees as the activities of the marker enzymes citrate synthase (matrix) and cytochrome c oxidase (respiratory chain). Therefore, the reduction of cellular respiration was mainly caused by a decrease in mitochondrial content per cell. The functional integrity of mitochondria was preserved, apart from the slight degree of cytochrome c release, either through a pore formed by the oligomerisation of BAK in coupled mitochondria or by permeability transition of a small fraction of injured mitochondria.
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PMID:Mitochondrial function in glucocorticoid triggered T-ALL cells with transgenic bcl-2 expression. 1224 Oct 83

Base excision repair is the main pathway for repair of oxidative base lesions in DNA. Mammalian cells must maintain genomic stability in their nuclear and mitochondrial genomes, which have different degrees of vulnerability to DNA damage. This study quantifies DNA glycosylase activity in mitochondria and nucleus from C57/BL 6 mouse tissues including brain, liver, heart, muscle, kidney, and testis. The activities of oxoguanine DNA glycosylase (OGG1), uracil DNA glycosylase, and endonuclease III homologue 1 (NTH1) were measured using oligonucleotide substrates with DNA lesions specific for each glycosylase. Mitochondrial content was normalized to citrate synthase activity and mitochondrial function was assessed by measuring cytochrome c oxidase (COX) activity. In nuclear and mitochondrial extracts, the highest DNA glycosylase activities were in testis. Brain and heart, tissues with the highest oxidative load, did not have higher levels of OGG1 or NTH1 activity than muscle or kidney, which are more glycolytic tissues. In general, mitochondrial extracts have lower DNA glycosylase activity than nuclear extracts. There was no correlation between glycosylase activities in the mitochondrial extracts and COX activity, suggesting that DNA repair enzymes may be regulated by a mechanism different from this mitochondrial enzyme.
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PMID:Base excision repair capacity in mitochondria and nuclei: tissue-specific variations. 1246 54

This study evaluated the link between swimming endurance and condition of Atlantic cod Gadus morhua that had been fed or starved during the 16 weeks preceding the tests, and assessed whether muscle metabolic capacities explain such links. The condition factor [(somatic mass x fork length(-3))x100] of starved cod was 0.54+/-0.1 whereas that of fed cod was 0.81+/-0.1. In white and red muscle, we measured four glycolytic enzymes: phosphofructokinase (PFK), pyruvate kinase (PK), creatine kinase (CK) and lactate dehydrogenase (LDH), two mitochondrial enzymes: cytochrome c oxidase (CCO) and citrate synthase (CS), a biosynthetic enzyme, nucleoside diphosphate kinase (NDPK), glycogen and protein levels and water content. Muscle samples were taken at three positions along the length of the fish; starvation affected the metabolic capacities of white muscle more than those of red muscle. The levels of glycolytic enzymes and glycogen changed more in white than red muscle during starvation. Both in fed and starved cod, muscle metabolic capacities varied with position along the fish; starvation reduced this longitudinal variation more in white than red muscle. In white muscle of fed cod, the glycolytic enzyme levels increased from head to tail, while in starved cod this longitudinal variation disappeared. In red muscle mitochondrial enzyme levels were highest in the caudal sample, but fewer differences were found for glycolytic enzymes. Swimming endurance was markedly affected by fish condition, with starved fish swimming only 30% of the time (and distance) of fed fish. This endurance was closely linked with the number of burst-coast movements during the test and the activity of CCO and LDH in white muscle. The number of burst-coast movements was significantly linked with condition factor and PFK activity in caudal red muscle and gill arch mass. Our data indicated that cod use both glycolytic and oxidative capacities to support endurance swimming. Furthermore, swimming endurance is linked with the metabolic capacities of red and white muscle.
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PMID:Condition, prolonged swimming performance and muscle metabolic capacities of cod Gadus morhua. 1250 71


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