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:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In untrained subjects, strenuous exercise provokes the appearance of oxidant stress markers in blood and muscle. On the other hand, trained muscle is resistant to oxidant stress unless exercise challenges the muscle glycogen supply. It is not known whether chronic high-intensity exercise alters the susceptibility of skeletal muscle to oxidant stress, whether there are gender-related differences in markers of oxidant stress, or whether elevating muscle glycogen stores by increasing dietary carbohydrate can minimize any exercise-related oxidant stress. To address these issues, collegiate rowers (12 men, 11 women) were randomly assigned to a moderate-(MOD, 5 g/kg body wt) or high-carbohydrate (HI, 10 g/kg) diet in a double-blind design and underwent strenuous training for 4 wk. Training in the A.M. was 40 min at 70% maximal O2 consumption (VO2); in the P.M. it was either three 2,500-m time trials (to assess power output) or aerobic and lactate tolerance training. Total daily training time was 65 min at 70% maximal VO2 and 38 min at > or = 90% maximal VO2. Thrice-weekly morning blood samples were assayed for serum creatine kinase (CK), plasma thiobarbituric acid-reactive substances (TBARS), and serum beta-glucuronidase (beta-Gluc). Weekly muscle biopsies were obtained for analysis of glycogen and, when tissue sample quantity allowed, TBARS. HI rowers produced more power and improved power more (10.7 +/- 1.0 vs. 1.6 +/- 1.6%) over the 4 wk than did the MOD rowers. Preexercise muscle glycogen concentration was maintained at 119 mmol/kg in MOD but increased 65% in HI rowers (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:No evidence of oxidant stress during high-intensity rowing training. 833 41

The effect of curcumin on the biochemical changes induced by isoproterenol (ISO) administration in rats was examined. ISO (300 mg Kg-1 administered subcutaneously twice at an interval of 24 h) caused a decrease in body weight and an increase in heart weight, water content as well as in the levels of serum marker enzymes viz creatine kinase (CK), lactate dehydrogenase (LDH) and LDH1 isozyme. It also produced electrocardiographic changes such as increased heart rate, reduced R amplitude and ST elevation. Curcumin at a concentration of 200 mg.Kg-1, when administered orally, showed a decrease in serum enzyme levels and the electrocardiographic changes got restored towards normalcy. Myocardial infarction was accompanied by the disintegration of membrane polyunsaturated fatty acids expressed by increase of thiobarbituric acid reactive substance (TBARS), a measure of lipid peroxides and by the impairment of natural scavenging, characterized by the decrease in the levels of superoxide dismutase, catalase, glutathione peroxidase, ceruloplasmin, alpha tocopherol, reduced glutathione (GSH) and ascorbic acid. The oral pretreatment with curcumin two days before and during ISO administration decreased the effect of lipid peroxidation. It was shown to have a membrane stabilizing action by inhibiting the release of beta-glucuronidase from nuclei, mitochondria, lysosome and microsome. Curcumin pre- and co-treatment decreased the severity of pathological changes and thus, could have a protective effect against the damage caused by myocardial infarction (MI).
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PMID:Protective role of curcumin against isoproterenol induced myocardial infarction in rats. 885 58

This study investigated the effects of chronic muscle inflammation on indices of antioxidant status and muscle injury after eccentric exercise. Eight subjects each performed 70 maximal voluntary eccentric muscle actions on an isokinetic dynamometer, using the knee extensors of a single leg. Venous blood samples were collected into serum and EDTA tubes 5 and 3 days before exercise, immediately before exercise, and then again on days 3, 4, 5, 6, 7, 10 and 12 after the bout. Needle biopsies were taken from the vastus lateralis of six subjects, a week before exercise (baseline), and again on days 4 and 7 post-exercise. The concentrations of malondialdehyde in plasma and muscle were used as markers of lipid peroxidation. Creatine kinase activity, beta-glucuronidase activity and total antioxidant capacity were determined in serum. In muscle, aqueous and bound total antioxidant capacity, the aqueous sulphydryl concentration, and beta-glucuronidase and glucose-6-phosphate dehydrogenase activity were determined. No changes were detected in serum total antioxidant capacity, serum creatine kinase and beta-glucuronidase after the baseline biopsy. After exercise serum creatine kinase and beta-glucuronidase were elevated although other serum measures were unchanged. In muscle, aqueous and bound total antioxidant capacity, sulphydryls, glucose-6-phosphate dehydrogenase and beta-glucuronidase were all elevated. Despite evidence of inflammation in this study, muscle antioxidant status was not compromised, and malondialdehyde was unaltered in muscle and plasma. Therefore, this study provides no evidence that chronic muscle inflammation compromises antioxidant status or increases lipid peroxidation.
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PMID:Changes in indices of antioxidant status, lipid peroxidation and inflammation in human skeletal muscle after eccentric muscle actions. 985 13

To test the effect of low ambient temperature on muscular strain and possible development of muscle injuries, male Sprague-Dawley rats (n = 35) were exercised at a speed of 15 m min-1 on a treadmill at a 6 degrees inclination for 1.5 h in a warm (22 degrees C) or a cold (-10 degrees C) environment. Blood and tissue samples were collected 0 and 48 h postexercise. Blood glucose, lactate, pyruvate, cortisol, epinephrine (E) and norepinephrine (NE) were determined to investigate the effect on energy metabolism. To estimate the degree of physical strain, possible muscle injury and regenerative processes of muscles in response to exercise in the cold, serum creatine kinase (CK), lactate dehydrogenase (LDH), muscle beta-glucuronidase and prolyl-4-hydroxylase (PH) activities were measured. In addition, histology of the hindlimb muscles m. soleus and m. tibialis anterior was examined. In general, the circulating level of metabolic substrates during exercise were unaffected by the exercise and independent of ambient temperature. Plasma cortisol increased significantly during exercise (P < 0.01), but was unaffected by the thermal strain. Of the myocellular enzymes, serum CK increased by 100% (P < 0.01) and LDH by 93% (P < 0.05) during exercise in the cold compared with exercise in warm, indicating a higher physical strain. However, exercise in the cold did not result in muscle injuries as judged by the unaltered muscular beta-glucuronidase, PH levels and muscle morphology. It is concluded that the exercise type and intensity used caused stress that was independent of the ambient temperature. In addition, the rats were able to maintain unaltered circulating levels of energy substrates also in the cold. Finally, exercise in the cold increased muscular strain but did not result in muscle injuries.
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PMID:Submaximal exercise in the cold: does cooling potentiate the development of muscle injuries in the rat? 997 24

Eccentric muscle contraction causes fibre injury associated with disruption of the myofibrillar cytoskeleton. The medicinal plant Panax ginseng C.A. Meyer, known for its therapeutic properties, was studied to explore its protective effects after eccentric contraction. A crude extract and a standardised extract (G115) of different saponin compositions were tested as to their efficacy in reducing lipid peroxidation, inflammation and release of myocellular proteins after the realisation of an eccentric contraction protocol on a rat treadmill. Plasma creatine kinase (CK) levels were significantly reduced by approximately 25% after ingestion of both extracts of ginseng. Both extracts reduced lipid peroxidation by approximately 15% as measured by malondialdehyde levels. beta-Glucuronidase concentrations and glucose-6-phosphate dehydrogenase (G6PDH) levels, which can be considered markers of inflammation, were also significantly reduced. The values of beta-glucuronidase were increased from 35.9+/-1.5 to 128.4+/-8.1 in vastus and to 131.1+/-12.1 U x g(-1) in rectus, the protection due to ginseng administration being approximately 40% in both muscles. Both extracts appeared to be equally effective in reducing injuries and inflammation caused by eccentric muscle contractions.
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PMID:Protective effects of Panax ginseng on muscle injury and inflammation after eccentric exercise. 1170 93

Diets rich in natural antioxidants are associated with reduced risk of heart diseases. This study was aimed to evaluate the preventive role of naringin on cardiac troponin T (cTnT), lactate dehydrogenase (LDH)-isoenzyme, cardiac marker enzymes, electrocardiographic (ECG)-patterns and lysosomal enzymes in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85mg/kg) at an interval of 24h for 2 days showed a significant increase in the levels of cTnT, intensity of the bands of LDH-isoenzyme (LDH1 and LDH2) and the activities of cardiac marker enzymes such as creatine kinase-MB (CK-MB), creatine kinase (CK), LDH, aspartate transaminase (AST) and alanine transaminase (ALT) in serum with subsequent decrease in the activities of CK, LDH, AST and ALT in the heart and alterations in ECG-patterns. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly in serum and the heart of ISO-induced rats, but the activities of beta-glucuronidase and cathepsin-D were decreased significantly in the lysosomal fraction of the heart. Pretreatment with naringin (10, 20 or 40mg/kg) daily for a period of 56 days positively altered the levels of cTnT, intensity of the bands of the LDH1 and LDH2-isoenzyme and the activities of cardiac marker enzymes, ECG-patterns and lysosomal hydrolases in ISO-induced rats. Thus, naringin possess cardioprotective effect in ISO-induced MI in rats.
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PMID:Preventive effect of naringin on cardiac markers, electrocardiographic patterns and lysosomal hydrolases in normal and isoproterenol-induced myocardial infarction in Wistar rats. 1718 15

Altered membrane integrity has been suggested as a major factor in the development of cellular injury during myocardial necrosis. The present study was designed to investigate the effect of diosgenin on lysosomal hydrolases, membrane-bound enzymes, and electrolytes during isoproterenol (ISO)-induced myocardial necrosis in rats. Animals were pretreated with DIOS (80 mg/kg) for a period of 35 days. Myocardial infarction was experimentally induced with ISO (85 mg/kg) twice at 24 h interval. Experimental myocardial infarction was evidenced with marked elevation of creatine kinase-MB (CK-MB) in serum with concomitant increase in lipid peroxidation (plasma thiobarbituric acid reactive substances (TBARS) and hydroperoxides (HP)). Activity of lysosomal hydrolases (beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-D-galactosidase, cathepsin D, and acid phosphatase) was found to be increased in serum and heart tissue of ISO-alone treated animals. DIOS (80 mg/kg) pretreated groups showed significant decrease in CK-MB, lipid peroxidation, and lysosomal hydrolases activity. The membrane-bound enzymes such as Ca2+-ATPase and Mg2+-ATPase activity was increased and Na+/K+-ATPase activity was decreased in the heart tissues of ISO-alone treated animals. These enzyme alterations lead to the change in the electrolytes content such as sodium, potassium, and calcium in the heart tissue. However, DIOS (80 mg/kg) pretreatment reversed the membrane-bound enzymes activity and thereby maintained the normal electrolyte concentration. These results suggest the protective action of diosgenin in ISO-induced myocardial infarction. The salubrious effect observed in this study might be due to the antioxidant and membrane stabilizing potential of diosgenin.
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PMID:Antilipoperoxidative and membrane stabilizing effect of diosgenin, in experimentally induced myocardial infarction. 1923 76

This study was aimed to evaluate the preventive effect of gallic acid on lysosomal enzymes in isoproterenol treated myocardial infarcted rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily for a period of 10 days. After the treatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h. The activity of creatine kinase-MB and lactate dehydrogenase were increased significantly (P<0.05) in the serum of isoproterenol induced cardiotoxic rats. The levels of lipid peroxidation products (thiobarbituric acid reactive substances, lipid hydroperoxides) were significantly (P<0.05) increased and the level of reduced glutathione was significantly (P<0.05) decreased in the plasma and heart of isoproterenol induced cardiotoxic rats. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and D) were increased significantly (P<0.05) in the serum and heart of isoproterenol induced cardiotoxic rats. Isoproterenol induction also resulted in decreased stability of membranes, which was reflected by lowered activities of beta-glucuronidase and cathepsin-D in lysosomal fraction. Pretreatment with gallic acid (15 mg/kg) to isoproterenol treated rats significantly (P<0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes. Oral treatment with gallic acid (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study show that gallic acid prevents the lysosomal membrane damage against isoproterenol induced cardiac damage and brought back the activities of lysosomal enzymes to near normal levels. The observed effects of gallic acid are due to antilipoperoxidative and antioxidant effects.
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PMID:Gallic acid prevents lysosomal damage in isoproterenol induced cardiotoxicity in Wistar rats. 1945 May 77

As women enter menopause, the concentration of estrogen and other female hormones declines. This hormonal decrease has been associated with a number of negative outcomes, including a greater incidence of injury as well as a delay in recovery from these injuries. Over the past two decades, our understanding of the protective effects of estrogen against various types of injury and disease states has grown immensely. In skeletal muscle, studies with animals have demonstrated that sex and estrogen may potentially influence muscle contractile properties and attenuate indices of post-exercise muscle damage, including the release of creatine kinase into the bloodstream and activity of the intramuscular lysosomal acid hydrolase, beta-glucuronidase. Furthermore, numerous studies have revealed an estrogen-mediated attenuation of infiltration of inflammatory cells such as neutrophils and macrophages into the skeletal muscles of rats following exercise or injury. Estrogen has also been shown to play a significant role in stimulating muscle repair and regenerative processes, including the activation and proliferation of satellite cells. Although the mechanisms by which estrogen exerts its influence upon indices of skeletal muscle damage, inflammation and repair have not been fully elucidated, it is thought that estrogen may potentially exert its protective effects by: (i) acting as an antioxidant, thus limiting oxidative damage; (ii) acting as a membrane stabilizer by intercalating within membrane phospholipids; and (iii) binding to estrogen receptors, thus governing the regulation of a number of downstream genes and molecular targets. In contrast to animal studies, studies with humans have not as clearly delineated an effect of estrogen on muscle contractile function or on indices of post-exercise muscle damage and inflammation. These inconsistencies have been attributed to a number of factors, including age and fitness level of subjects, the type and intensity of exercise protocols, and a focus on sex differences that typically involve factors and hormones in addition to estrogen. In recent years, hormone replacement therapy (HRT) or estrogen combined with exercise have been proposed as potentially therapeutic agents for postmenopausal women, as these agents may potentially limit muscle damage and inflammation and stimulate repair in this population. While the benefits and potential health risks of long-term HRT use have been widely debated, controlled studies using short-term HRT or other estrogen agonists may provide future new and valuable insights into understanding the effects of estrogen on skeletal muscle, and greatly benefit the aging female population. Recent studies with older females have begun to demonstrate their benefits.
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PMID:The influence of estrogen on skeletal muscle: sex matters. 2002 Jul 86

We evaluated the preventive effect of caffeic acid (CA) on lysosomal enzymes in isoproterenol (ISO)-treated myocardial infarcted rats. Male albino Wistar rats were pretreated with CA (15 mg/kg) daily for a period of 10 days. After the pretreatment period, ISO (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h. The activity of serum creatine kinase-MB and lactate dehydrogenase was increased significantly (P < 0.05) in ISO-induced myocardial infarcted rats. The levels of plasma thiobarbituric acid reactive substances and lipid hydroperoxides were significantly (P < 0.05) increased, and the level of plasma-reduced glutathione was significantly (P < 0.05) decreased in ISO-induced myocardial infarcted rats. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly (P < 0.05) in the serum and heart of ISO-induced myocardial infarcted rats. ISO induction also resulted in decreased stability of membranes, which was reflected by lowered activities of beta-glucuronidase and cathepsin-D in different fractions except cytosol. Pretreatment with CA (15 mg/kg) to ISO-treated rats significantly (P < 0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes in the serum, heart, and subcellular fractions. Oral treatment with CA (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study showed that CA prevented the lysosomal membrane damage against ISO-induced myocardial infarction. The observed effects of CA are due to membrane-stabilizing, antilipo peroxidative, and antioxidant effects.
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PMID:Preventive effect of caffeic acid on lysosomal dysfunction in isoproterenol-induced myocardial infarcted rats. 2039 26


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