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)

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

To investigate the effects of strenuous forced exercise on the course and complications of a bacterial infection and on myocardial responses and performance capacity, rats with tularemia (characterized by pyogranulomatous hepatic and splenic lesions) were exercised by swimming on days 0-6 of infection. Levels of glutamic oxaloacetic and pyruvic transaminases in plasma, densities of pyogranulomatous lesions, and bacterial counts in blood, liver, and spleen were similar in exercising and resting rats. Although a few exercising rats showed an unusual dissemination of infection, the antibody responses were similar in rest and exercise. Plasma concentrations of beta-glucuronidase, lysozyme and alpha 2-macrofetoprotein were higher with exercise, a result that indicated that more vigorous stress responses were elicited with exercise than with infection alone. Physical performance capacity was reduced by the infection, but forced daily exercise limited this reduction substantially and counteracted the myocardial protein-degrading effects of infection. Thus, exercise evoked normal training responses even during this generalized infection.
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PMID:The effects of strenuous exercise on infection with Francisella tularensis in rats. 707 93