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)

Disruption of cellular constituents including inhibition or "downregulation" of metabolic enzyme activity has been associated with free radical stress in locomotor muscle with acute, strenuous exercise. However, the effects of acute, strenuous exercise on important metabolic and antioxidant enzyme activity levels in the diaphragm are unknown. Twenty 4-month-old and twenty 24-month-old female Fischer-344 rats were divided at random into young exercised (YE; n = 10)/old exercised (OE; n = 10); young control (YC; n = 10)/old control (OC; n = 10) groups. Animals in both young and old exercise groups ran on a treadmill (10% uphill grade) for 40 min at approximately 75% of age group VO2 max. Immediately following the treadmill run, both exercise and control groups were euthanized with sodium pentobarbital. Costal (COD) and crural diaphragm (CRD) were quickly removed and frozen in liquid nitrogen. Lipid peroxidation was significantly increased (P < 0.05) in COD of YE vs. YC rats. Activity of the antioxidant enzyme glutathione peroxidase (GPX) was unaltered in the diaphragm by acute exercise (P > 0.05) in both age groups. There was a significant increase in superoxide dismutase (SOD) activity with exercise (P < 0.05). Post-hocs revealed SOD activity was approximately 20% greater (P = 0.066) in YE CRD only. Activities of the metabolic enzymes phosphofructokinase (PFK), succinate dehydrogenase (SDH), and citrate synthase (CS) were not affected by acute exercise in YE or OE. Strenuous exercise resulted in a small trend towards a decrease in 3-hydroxyacyl-CoA dehydrogenase (HADH) activity in YE COD (P = 0.115) and YE CRD (P = 0.082). We conclude that the employed bout of exercise induces some free radical stress, while metabolic enzymes are protected, in the diaphragm.
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PMID:Metabolic and antioxidant enzyme activities in the diaphragm: effects of acute exercise. 805 80

This study examined the effect of experimental hyper- and hypothyroidism on the superoxide dismutase, catalase and glutathione peroxidase activities of rat lymphoid organs (mesenteric lymph nodes, spleen and thymus) and muscles (soleus and gastrocnemius-white portion) for comparison. The capacity for the generation of reducing equivalents was also investigated: activities of glucose-6-phosphate dehydrogenase (pentose-phosphate pathway) and citrate synthase (Krebs cycle). Hyperthyroidism tended to enhance lipid peroxide content in all tissues. This effect may result from (1) a high capacity for the generation of reducing equivalents in cytosol and mitochondria and (2) a reduced activity of catalase in the lymphoid organs and of glutathione peroxidase in the muscles. The process of lipid peroxidation in these tissues caused by hyperthyroidism was probably slowed down by the augmentation of CuZn- and Mn-superoxide dismutase (Mn-SOD) activities observed under this condition. Hypothyroidism tended to diminish lipid peroxidation and did not affect citrate synthase and glucose-6-phosphate dehydrogenase activities in the lymphoid organs and muscles. Low levels of thyroid hormones tended to diminish Mn-SOD and glutathione peroxidase activities. These findings show that the thyroid hormones might be able to regulate the activities of CuZn- and Mn-SOD, and catalase and glutathione peroxidase in the lymphoid organs and skeletal muscles.
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PMID:Control of superoxide dismutase, catalase and glutathione peroxidase activities in rat lymphoid organs by thyroid hormones. 813 54

These experiments examined the influence of exercise intensity and duration on antioxidant enzyme activity in locomotor muscles differing in fiber type composition. Nine groups of female Sprague-Dawley rats (age 120 days) exercised 4 days/wk on a motor-driven treadmill for 10 wk. The impact of three levels of exercise intensity (low, moderate, and high: approximately 55, approximately 65, and approximately 75% of maximal oxygen consumption, respectively) and exercise duration (30, 60, and 90 min/day) was assessed. Sedentary animals served as controls. Oxidative capacity in the soleus and white and red gastrocnemius was assessed by measurement of citrate synthase (CS) activity, and antioxidant capacity was evaluated by assay of total superoxide dismutase, catalase, and total glutathione peroxidase (GPX) activities. In all muscles, CS activity increased as a function of exercise duration. Furthermore, in the soleus and white gastrocnemius, the magnitude of the training-induced increase in CS activity was directly related to exercise intensity. In contrast, the peak increase in CS activity in the red gastrocnemius was relatively independent of exercise intensity. Catalase activity was not increased (P > 0.05) in any muscle with training. Training-induced changes in superoxide dismutase and GPX activities were muscle specific; specifically, exercise training significantly (P < 0.05) increased superoxide dismutase activity in the soleus as a function of exercise duration up to 60 min/day. Conversely, training-induced significant (P < 0.05) increases in GPX activity occurred in red gastrocnemius only; the magnitude of the GPX increase was directly related to exercise duration but relatively independent of intensity. These data demonstrate that exercise training-induced changes in muscle antioxidant enzymes are muscle specific.
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PMID:Influence of exercise and fiber type on antioxidant enzyme activity in rat skeletal muscle. 814 92

The effects of endurance training on tissue antioxidant and oxidative enzyme activities were determined in heart, liver, and five skeletal muscles of female rats. Rats were fed either normal (+E) or vitamin E free (-E) diets for 16 wk. For the final 8 wk, subgroups of +E and -E diet animals were trained by treadmill running at 40 m.min-1, 15% grade for 60 min.d-1. No significant differences in training abilities were observed between diet groups. Endurance training significantly increased citrate synthase (CS) activity in all skeletal muscles for both the +E and -E diet animals with no significant difference in degree of response between diet groups. Neither vitamin E deprivation, training, or their combination generally affected the activities of the antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPX) in skeletal muscles, heart, or liver of the animals. These results suggest that despite an anticipated increase in free radical induced tissue "oxidative stress" brought about by a combination of vitamin E deprivation and endurance training, antioxidant enzyme adaptations were not evident and the response of citrate synthase to training was not impaired in female rats.
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PMID:Antioxidant and oxidative enzyme adaptations to vitamin E deprivation and training. 818

We examined the relationship between the intensity and duration of exercise training and the up-regulation of diaphragmatic oxidative and antioxidant enzyme activities. Nine groups of rats exercised for 10 weeks (4 days/week). Groups of animals exercised at three intensities (low, moderate, and high); at each exercise intensity, a group of animals ran at one of three exercise durations (30, 60, and 90 min/day). Sedentary animals served as controls. Muscle oxidative capacity was assessed by citrate synthase (CS) activity while antioxidant capacity was evaluated by total superoxide dismutase (SOD) and total glutathione peroxidase (GPX) activities. All intensities and durations of exercise training promoted significant (P < 0.05) increases in costal diaphragmatic CS, SOD, and GPX activities. Increases in costal CS, SOD, and GPX activity were independent of the exercise intensity and duration. High and moderate intensity exercise of 90 min duration significantly elevated (P < 0.05) crural diaphragm CS activity. Further, high and moderate intensity exercise of durations > or = 60 min promoted significant (P < 0.05) increases in crural diaphragm SOD activities. Exercise did not influence (P > 0.05) crural diaphragm GPX activity. We conclude that the training threshold for up-regulation of oxidative and antioxidant enzyme activities differs between the costal and crural diaphragm.
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PMID:Regional training-induced alterations in diaphragmatic oxidative and antioxidant enzymes. 819 Oct 43

Parkinson's disease (PD) is characterized mainly by a loss of nigrostriatal dopamine neurons. Thus far, the actual physiopathology of PD remains uncertain, although recent studies have found decreased activity of complex I, one of the enzymatic units of the mitochondrial respiratory chain, in various tissues of PD patients. Because most, if not all, of PD patients are treated chronically with levodopa, the precursor of dopamine, and because we have shown previously that catecholamines may alter mitochondrial respiration, we assessed the effects of chronic administration of levodopa on complex I activity in rat brain. We found that chronic administration of levodopa, at a dose used in PD patients, caused a significant reduction in complex I activity while it did not affect the activities of complex II, complex IV, and citrate synthase. Reduction in complex I activity correlated well with catecholamine innervation as the reduction was observed mainly in the striatum and substantia nigra and to a lesser extent in the frontal cortex but not in the cerebellum. Moreover, the levodopa-induced decrease of complex I activity was reversible since activities at 1, 3, and 7 days after the last injection showed a progressive return to control values. Incubation of whole brain mitochondria in vitro showed that both levodopa and dopamine inhibit complex I activity in a dose- and time-dependent manner. In contrast, other compounds such as homovanillic acid, 3,4-dihydroxyphenylacetic acid, and 3-O-methyl-dopa were minimally effective. Reduced glutathione, ascorbate, superoxide dismutase, and catalase prevented the effect of levodopa and dopamine on complex I. Various inhibitors of monoamine oxidase also prevented the effect of dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic levodopa administration alters cerebral mitochondrial respiratory chain activity. 823 66

Controversy exists as to the effect of endurance training on myocardial antioxidant enzyme activity. These experiments sought to clarify this issue by examining antioxidant enzyme activities in the rat ventricular myocardium in response to different intensities and durations of exercise training. Female Fischer-344 rats (120 days old) were assigned to either a sedentary control group or one of nine exercise training groups. Animals were exercised on a motorized treadmill for 10 wk; combinations of three durations (30, 60, and 90 min/day), and three levels of exercise intensity (low, moderate, and high) were studied. Exercise training did not alter (P > 0.05) citrate synthase, catalase, or glutathione peroxidase activities in the right or left ventricle. In contrast, high-intensity exercise (all durations) and moderate-intensity exercise (90 min/day) resulted in a significant increase (P < 0.05; +28-30%) in right ventricular superoxide dismutase (SOD) activity. Similarly, high-intensity exercise training (all durations) resulted in a significant elevation (P < 0.05; +14-26%) of left ventricular SOD activity. Furthermore, low- and moderate-intensity exercise training of long duration (i.e., 60-90 min/day) resulted in significant increases (P < 0.05; +10-23%) in left ventricular SOD activity. These data support the hypothesis that high-intensity exercise (> or = 30 min/day) or moderate-intensity exercise of long duration (> or = 60 min/day) is effective in upregulating SOD activity in the ventricular myocardium.
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PMID:Rigorous exercise training increases superoxide dismutase activity in ventricular myocardium. 828 49

Inhibition of metabolic enzyme activity has been associated with free radical stress in locomotor muscle with prolonged or intense exercise. However, it is not known whether such alterations with acute exercise in skeletal muscle are influenced by muscle fiber type or age. Twenty 4-mo-old and twenty 24-mo-old female Fischer-344 rats were divided at random into young exercised (YE; n = 10), old exercised (OE; n = 10), young control (YC; n = 10), and old control (OC; n = 10) groups. Animals in both YE and OE groups ran on a treadmill (10% uphill grade) for 40 min at approximately 75% of each age-group's maximal O2 consumption. Immediately after the treadmill run, white gastrocnemius (WG), red gastrocnemius (RG), and soleus (SOL) muscles were removed and quick-frozen in liquid nitrogen. Malondialdehyde was significantly increased (P < 0.05) in RG of YE vs. YC rats. Glutathione peroxidase activity was significantly elevated (P < 0.05) in the WG of YE rats. Analysis of variance revealed a significant over-all increase in superoxide dismutase activity with exercise. Activities of phosphofructokinase (PFK), citrate synthase, succinate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase were unchanged (P > 0.05) with acute exercise in the SOL. However, PFK activity was decreased in the WG by 60% in OE but only 33% in YE, and in the RG by 41% in OE but only 21% in YE. We conclude that maximal glycolytic flux in the gastrocnemius may be adversely affected by acute exercise, and this effect was more pronounced in the 24-mo-old group.
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PMID:Acute exercise and skeletal muscle antioxidant and metabolic enzymes: effects of fiber type and age. 828 76

The alterations of superoxide dismutase iso-enzyme (Cu,Zn-SOD and Mn-SOD) activities, contents, and mRNA expressions with aging were studied in rat soleus muscle (SO) and extensor digitorum longus muscle (EDL). The activity and content of Cu,Zn-SOD in both muscles were significantly higher in old rats (24 months old) than in young rats (4 months old), whereas those of Mn-SOD showed no difference between young and old rats. After normalization to citrate synthase (CS) activity, however Mn-SOD/CS ratio in SO also showed the age-related increase. Moreover, the activities of other major antioxidant enzymes, glutathione peroxidase (GPX) and catalase (CAT), indicated age-related increases only in SO. As for the expressions of mRNAs for SOD iso-enzymes, that of Cu,Zn-SOD in either muscle showed no significant change with aging, unlike its activity and content, although that of Mn-SOD was decreased with aging only in EDL. Thus, aging appeared to raise the level of antioxidant enzyme system in rat skeletal muscle. However, the resistance of Cu,Zn-SOD and Mn-SOD to oxidative stress accompanied by aging was different, the former being obviously greater than the latter. Such changes also differed in muscle fiber type suggesting that fast-twitch fibers are more susceptible to age-related oxidative stress than slow-twitch fibers.
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PMID:Alterations of superoxide dismutase iso-enzyme activity, content, and mRNA expression with aging in rat skeletal muscle. 871 78

The effects of 8 wk of 35 min of aerobic cycle training (3 times/wk) on indexes of male and female human vastus lateralis muscle antioxidant status were investigated. Training resulted in significant elevations in whole body maximal O2 consumption and muscle citrate synthase activity. Despite this, muscle superoxide dismutase, catalase, and glutathione peroxidase activities were not significantly altered by the training protocol. In addition, training did not affect muscle vitamin E (alpha- and gamma-tocopherol) concentrations. Glutathione status determined as the concentrations of reduced glutathione (GSH), oxidized glutathione (GSSG), total glutathione (GSH + 2 x GSSG), and GSH/GSSG ratio was unaffected by the training protocol. There were no significant differences between males and females in any indexes of muscle antioxidant status. These results indicate that the moderate aerobic training typically performed by regularly exercising humans did not positively alter endogenous antioxidant status. This suggests that short-term aerobic training increases capacity for flux through the citric acid cycle without necessarily increasing the ability to handle potential free radicals generated by the enhanced electron flux.
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PMID:Lack of antioxidant adaptation to short-term aerobic training in human muscle. 889 71


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