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)

Dogs were given gentamicin (10 mg/kg) intramuscularly every 8 hr for 10 days. Levels of serum creatinine rose by day 6 (0.91 +/- 0.08 vs. 0.75 +/- 0.02 mg/dl for controls, P less than 0.05) and of blood urea nitrogen by day 8 (24.3 +/- 4.80 vs. 16.1 +/- 0.90 mg/dl for controls, P less than 0.05). Gentamicin nephrotoxicity occurred earlier and was more marked when furosemide (2 mg/kg) was added: the level of serum creatinine by day 6 was 1.62 +/- 0.25 mg/dl (P less than 0.05), and the level of blood urea nitrogen by day 8 was 181 +/- 23.5 mg/dl (P less than 0.01). Elevations in the activities of the urinary enzymes beta-glucuronidase, N-acetyl-beta-glucosaminidase, and muramidase preceded rises in levels of serum creatinine and blood urea nitrogen. Examination of serial percutaneous renal biopsy specimens showed that gentamicin administration was associated with hyaline droplet degeneration, lysosomal changes, and, later, cell necrosis (primarily of the proximal tubules). Changes in renal morphology were more severe and occurred earlier when furosemide was administered concomitantly. In summary, furosemide enhanced gentamicin nephrotoxicity. Enzymuria was an early sign of gentamicin nephrotoxicity.
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PMID:Furosemide enhancement of experimental gentamicin nephrotoxicity: comparison of functional and morphological changes with activities of urinary enzymes. 50 Nov 48

The labilizing effect of gentamicin, an aminoglycoside antibiotic, on isolated rat kidney lysosomes was investigated. The light-scattering behavior of lysosomal suspensions and the release of lysosomal acid hydrolase enzymes (acid phosphatase, beta-glucuronidase and muramidase) from incubated lysosomal suspensions, in the presence of gentamicin, were used as indices of lysosomal membrane labilization. Gentamicin was found to cause a decrease in light absorbance and a release of lysosomal acid hydrolases, which indicate lysosomal membrane swelling. In the presence of selenium, in the form of potassium selenate, the decrease in light absorbance of lysosomal suspensions and the release of lysosomal acid hydrolases from isolated lysosome particles were reduced markedly. This suggests that selenium protects against gentamicin-induced lysosomal membrane labilization. The possible mechanisms of protection by selenium are discussed.
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PMID:Studies on gentamicin-induced labilization of rat kidney lysosomes in vitro. Possible protection by selenium. 662 37

Gentamicin has been shown to induce renal tubular damage in man and laboratory animals and to result in elevated urinary excretion of some enzymes associated with specific cell regions in the kidney. In the present investigation, the possible protective effect of selenium against gentamicin-induced renal damage was tested by measuring the urinary excretion of some enzymes in the presence and absence of selenium. Our results show that a prior subcutaneous injection of selenium to rats for two days followed by a simultaneous S.C. injection of gentamicin and selenium resulted in a marked reduction in the excretion of such biochemical systems as the urine volume, urinary proteins, alkaline and acid phosphatases, beta-glucuronidase, muramidase, and glutamate dehydrogenase. Renal functional studies revealed that selenium-treated rats suffered less adverse effects compared to rats treated with gentamicin alone. Urinary acid phosphatase, beta-glucuronidase and muramidase, the three lysosomal enzymes tested, appeared to respond most readily to protection by selenium.
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PMID:Protection by selenium against gentamicin-induced acute renal damage in the rat. 672 37

A total of 169 Escherichia coli strains were isolated from cows with cases of clinical mastitis. beta-Glucuronidase production, serum sensitivity, and susceptibility to selected antibacterials were analyzed using the fluorometric beta-glucuronidase assay. About 89% (150 of 169) of the isolates tested positive for beta-glucuronidase. Of these isolates producing beta-glucuronidase, 102 (68%) were resistant or moderately resistant to bovine serum. The antibacterial susceptibility of 96 isolates was tested in broth and milk. There was a significant shift from lower fluorometric minimum inhibitory concentration for tetracycline, sulfadoxin-trimethoprim, enrofloxacin, and gentamicin in broth to higher fluorometric minimum inhibitory concentration in milk. Serum sensitivity and susceptibility to tested antibacterials in broth or in milk were not related. Gentamicin and sulfadoxin-trimethoprim seemed to be more potent in mastitic milk than in normal milk, suggesting a possible synergistic effect between these exogenous antibacterials and the indigenous antibacterial agents in mastitic milk.
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PMID:Mastitis-causing Escherichia coli: serum sensitivity and susceptibility to selected antibacterials in milk. 867 85