Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies with bacterial infections have demonstrated a reduced exercise capacity and equally pronounced catabolic responses in red and white skeletal muscle. In the present study, red skeletal muscle and heart ventricular muscle were compared in a S. typhimurium model in rats. Two days before median lethality was achieved, the activities of one oxidative (cytochrome c oxidase), one glycolytic (glyceraldehyde-3-phosphate dehydrogenase) and one lysosomal (beta-glucuronidase) enzyme were determined in the two tissues. The contents of protein, RNA and DNA were also determined. The oxidative and glycolytic capacity decreased 24-29% in red skeletal muscle but only 7-20% in the myocardium. However, the decrease in oxidative capacity in skeletal muscle and myocardium was statistically correlated. The protein synthetic capacity (RNA) also decreased and was correlated to the protein concentration in both tissues. This metabolic impairment of both skeletal and heart muscle probably contributes to the deterioration of the physical performance capacity previously observed to follow acute infectious diseases. This study emphasizes the importance of the choice of reference, such as 'wet' weight, DNA or the entire organ, when evaluating metabolic results in biologic tissues and that biochemical alterations in skeletal muscle biopsies in bacterial infections do not reflect alterations in myocardium reliably.
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PMID:Biochemical responses of the myocardium and red skeletal muscle to Salmonella typhimurium infection in the rat. 636 18

Mice with generalized influenza or tularemia of similar lethality were studied in an effort to compare biochemical responses of the myocardium during infections of viral and bacterial etiology. A progressive loss of body weight characterized the course of both infections. Accompanying this, the myocardial content of protein and the activities of lactate dehydrogenase, citrate synthase, and cytochrome c oxidase all decreased. However, myocardial protein degradation appeared earlier and was more pronounced in influenza, and the protein changes were accompanied by a rapid decline of myocardial RNA. Activation of acid hydrolases, such as cathepsin D and beta-glucuronidase, occurred in tularemia but not in influenza, whereas leakage of beta-glucuronidase into the plasma occurred in both infections. Conversely, there was a considerably greater activation of myocardial catalase in influenza. These findings suggested that different control mechanisms or metabolic pathways were operative in the degradation of myocardial constituents in influenza as compared with tularemia. The absence of histological signs of myocarditis in either infection appeared to exclude any direct local effects of an inflammatory process on myocardial cells. Since the infections were of comparable lethality (based upon the inoculated dose of organisms), the observed differences in pattern and extent of metabolic responses of the myocardium to these infections may be attributed to different pathophysiological mechanisms evoked by the different microorganisms.
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PMID:Sequential metabolic alterations in the myocardium during influenza and tularemia in mice. 674 1

For a study of the interactions of strenuous physical exercise (daily swimming to exhaustion) and a viral as compared with a bacterial infection with regard to the clinical course and the biochemical response of the myocardium, influenza and tularemia of similar lethality were used in mice. In both infections, expected infection-induced catabolic alterations in the ventricular myocardium were evident 2 days before median lethality was achieved, with a more pronounced wasting in influenza than in tularemia. Exercise before inoculation (preconditioning) was beneficial in that the catabolic effects of both infections were limited and lethality in influenza was reduced. Thus, the myocardial protein-degrading effect of influenza did not occur with preconditioning, and oxidative tissue enzyme activities decreased less. In tularemia, cytochrome c oxidase activity was fully preserved with preconditioning, and activation of catalase was less pronounced. Exercise during ongoing infection counteracted the infection-induced decrease in the activities of glycolytic and oxidative enzymes in tularemia, but lethality and bacterial counts in the spleen were uninfluenced. Conversely, exhaustive exercise in influenza increased lethality and had no significant effect on cardiac enzymes. These exercise models caused no major alterations in activation of lysosomal enzymes (beta-glucuronidase and cathepsin D).
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PMID:Modifying effects of exercise on clinical course and biochemical response of the myocardium in influenza and tularemia in mice. 674 2

The ventricular myocardium was studied in A/J mice and in Sprague-Dawley rats. In male mice, the ventricles were slightly larger and the specific activities of the lysosomal hydrolases, beta-glucuronidase, hexosaminidase, beta-galactosidase, and arylsulphatase, and the inner mitochondrial enzyme cytochrome c oxidase were substantially higher than in female mice. Orchiectomy abolished this sex difference. Testosterone administration induced myocardial hypertrophy and accretion of RNA and protein without altering the DNA, and substantial increases in the activities of the lysosomal hydrolases and cytochrome c oxidase. However, the mitochondrial membrane enzyme monoamine oxidase was unaffected by sex, orchiectomy, and testosterone administration. Heart lysosomes from male mice showed a smaller structure-linked latency of the lysosomal enzymes and a greater fragility of the lysosomal membrane to osmotic and mechanical stress than those from female mice. This sex difference was also abolished by orchiectomy and restored by testosterone replacement. Similar sex differences were observed in the rat with respect to heart size, acid hydrolase activities, and lysosomal enzyme latency and membrane stability. These findings indicate that endogenous androgens regulate myocardial cell growth, the activity of enzymes associated with lysosomes and the inner mitochondrial membrane, and some physiochemical properties of lysosomes.
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PMID:Testosterone-mediated sexual dimorphism of the rodent heart. Ventricular lysosomes, mitochondria, and cell growth are modulated by androgens. 704 2

In the present work, the promoter of the Arabidopsis thaliana nuclear gene COX5b-1, encoding subunit 5b of the mitochondrial cytochrome c oxidase, has been analysed. For this purpose, plants, stably transformed with different promoter fragments fused to the beta-glucuronidase reporter gene, have been obtained. Histochemical staining indicated that the COX5b-1 promoter directs expression in meristems and in vascular tissues of cotyledons, roots, and hypocotyls, as well as in anthers and pollen and the central leaf vein. Quantitative measurements in extracts prepared from different organs suggested that expression is higher in roots. The analysis of progressive upstream deletions of the promoter suggested the presence of negative regulatory elements, preferentially active in leaves, between nucleotides -609 and -387 from the translation start site. A further deletion down to nucleotide -195 completely abolished expression. The inclusion of sucrose or the cytokinin 6-benzylaminopurine in the culture medium induced COX5b-1 promoter-dependent beta-glucuronidase expression. This induction was observed with all constructs that produced beta-glucuronidase activity. Putative regulatory elements involved in the regulation of other genes were detected in the promoter fragment required for expression. A detailed analysis of these elements will help to elucidate the molecular mechanisms that participate in the expression of this and, possibly, other components of the cytochrome c-dependent respiratory pathway.
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PMID:The promoter of the Arabidopsis nuclear gene COX5b-1, encoding subunit 5b of the mitochondrial cytochrome c oxidase, directs tissue-specific expression by a combination of positive and negative regulatory elements. 1528 48


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