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:3.2.1.23 (beta-galactosidase)
14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the effect of acute myocardial infarction (AMI) on serum and urinary activity of beta-galactosidase and beta-glucuronidase (lysosomal enzymes) 40 patients were studied. Eighteen patients had acute myocardial infarction and 22 were assigned as controls. Three of the 18 patients with acute myocardial infarction died within 5 to 10 days after hospitalization. Although the serum and urinary beta-glucuronidase and serum beta-galactosidase activity was higher in patients with acute myocardial infarction when compared with the control subjects these differences did not achieve statistical significance. However, the mean values of urinary beta-galactosidase in the control and acute MI groups were 158.68 and 333.3 nmol/mg creatinine/hr, respectively (p less than 0.046). These findings indicate that there is a significant increase in the urine beta-galactosidase activity during the early phases of acute myocardial infarction.
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PMID:Serum and urinary beta-galactosidase and beta-glucuronidase activity in patients with acute myocardial infarction. 681 68

The renal function of workers occupationally exposed to cadmium (n = 148), to mercury vapor (n = 63) or to inorganic lead (n = 25) has been compared with that of workers with no occupational exposure to heavy metals (n = 88). A moderate exposure to lead (Pb-B < 62 microgram/100 ml) does not seem to alter renal function. Excessive exposure to cadmium increases the urinary excretion of both low- and high-molecular-weight proteins and of tubular enzymes. These changes are mainly observed in workers excreting more than 10 microgram Cd/g creatinine or with Cd-B above 1 microgram Cd/100 ml whole blood. Occupational exposure to mercury vapor induces glomerular dysfunction as evidenced by an increased urinary excretion of high-molecular-weight proteins and a slightly increased prevalence of higher beta 2-microglobulin concentration in plasma without concomitant change in urinary beta 2-microglobulin concentration. beta-galactosidase activity in blood and in urine is also increased. The likelihood of these findings is greater in workers with Hg-B and Hg-U exceeding 3 microgram/100 ml whole blood and 50 microgram/g creatinine, respectively. The hypothesis is put forward that the glomerular dysfunction induced by cadmium and mercury might result from an autoimmune mechanism.
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PMID:Assessment of renal function of workers exposed to inorganic lead, calcium or mercury vapor. 744 94

Genetically modified myogenic cells have a number of potentially relevant applications for gene therapy of genetic defects. Retroviral vectors proved to be a safe and efficient tool to transfer and express genes into satellite cells and their differentiated progeny, although muscle-specific regulation of the transferred gene is very difficult to achieve in a conventional vector framework. We modified a Moloney murine leukemia virus (MoMLV)-derived retroviral vector containing a bacterial beta-galactosidase (beta-Gal) reporter gene by inserting a muscle creatinine kinase (MCK) enhancer element into the U3 region of the viral long terminal repeat (LTR). The resulting vector (mLBSN) was transferred into cells of different histological origin, including undifferentiated murine and human myogenic cells, which were unable to express the transgene at detectable levels. Instead, gene expression from the modified LTR was obtained in a mouse myogenic cell line and in human primary satellite cells upon induction of differentiation into myotubes in culture, and correlated with the activation of the muscle differentiation program. beta-Gal-negative, mLBSN-transduced human satellite cells were also transplanted into the quadricep muscle of immunodeficient mice, where activation of the transgene expression was observed in vivo after differentiation and fusion into muscle fibers. These results show that retroviral vectors carrying LTRs modified in the enhancer sequences may be used to target tissue- and differentiation-specific gene expression into the muscle. For practical purposes, satellite cells engineered by muscle-specific retroviral vectors might represent an effective tool to deliver expression of a given gene product specifically into the muscle tissue, avoiding undesired protein accumulation in mononucleated cells. More generally, this type of vector might be useful whenever regulated expression of a transferred gene is necessary in a target cell or tissue.
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PMID:A retroviral vector containing a muscle-specific enhancer drives gene expression only in differentiated muscle fibers. 754 73

Various enzymatic urinary activities have been proposed to assess renal proximal tubule damage in children, including neonates. Nevertheless comprehensive knowledge on the developmental aspects of physiological enzymuria is limited, particularly with regard to lysosomal and brush border enzymuria. Urinary activities of two lysosomal enzymes, N-acetyl-beta-D-glucosaminidase (NAG) and beta-galactosidase (GAL), and of two brush border enzymes, alanine aminopeptidase (AAG) and gamma-glutamyltransferase (GGT) were comparatively investigated in normal prematures (n = 28), term neonates (n = 52), infants aged less than 2 years (n = 19) and children (n = 33), and compared to urinary excretion of beta 2-microglobulin (B2M). Enzymatic activities were assayed using either spectrophotometrical (NAG, AAP, GGT) fluorimetrical (GAL) or radioimmunological (B2M) methods, and were related to urinary creatinine excretion. Developmental profiles of both the studied lysosomal enzymes and of B2M were similarly characterized with significantly decreasing values from prematures (NAG 9.29 +/- 1.44, GAL 2.26 +/- 0.26 IU/mmol creatinine, indicated as mean +/- SEM) to term neonates (6,94 +/- 0.58 and 1.76 +/- 0.15 IU/mmol creatinine, respectively) and older infants and children. Lysosomal enzymatic urinary activities correlated linearly with a coefficient of r = 0.75, (p < 0.05), while correlations between each lysosomal enzymatic activity and B2M urinary excretion were weaker.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specific developmental profiles of lysosomal and brush border enzymuria in the human. 772 20

The activities of five lysosomal hydrolases--namely beta-glucuronidase, beta-hexosaminidase, beta-galactosidase, alpha-galactosidase, and alpha-mannosidase--were measured in the plasma and urine of children (ages, 7 to 15 years) with sickle cell anemia (n = 11) and controls (n = 11) from Jos, Nigeria. The presence of SS hemoglobin was confirmed by electrophoresis of red cell hemolysates. Albuminuria was absent in all of the patients with sickle cell anemia. The creatinine-indexed urinary activity level (units of enzyme activity/milligrams creatinine) and the fractional enzyme excretion (FEE) value, which is defined as the ratio of enzyme clearance to creatinine clearance, were determined for each of the five lysosomal enzymes and compared between the two groups. The mean FEE values for beta-glucuronidase and alpha-galactosidase in the sickle cell patients were 10- and 3.5-fold lower, respectively, than the corresponding control values, and these differences were statistically significant (p < .03) for both enzymes; however, beta-hexosaminidase, beta-galactosidase, and alpha-mannosidase levels in urine were not different between the two groups. When indexed to creatinine, a comparison of the urinary enzyme levels of control and sickle cell patients showed significant differences for beta-glucuronidase (p < .01) and alpha-galactosidase (p < .05) but not for the other three enzymes. Differences in level of plasma enzyme activity between control and sickle cell patients were not significant, except for alpha-galactosidase (p < .05), which was increased slightly (25%) in the sickle cell group. These data indicate that there may be abnormalities in the metabolism of lysosomal enzymes in the kidneys of patients with sickle cell anemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased urinary excretion of beta-glucuronidase in sickle cell anemia in Nigeria. 777 Jun 45

The early renal function parameters (RFP), i.e. urinary alanine aminopeptidase (AAP), beta-galactosidase (beta GAL), N-acetyl-beta-D-glucosaminidase (NAG), retinol-binding protein (RBP), albumin (ALB), total protein (TP) and the conventional RFP plasma creatinine were assessed in 8 patients before and during treatment with the nephrotoxic antitumor agent cis-platin. Plasma creatinine increased during treatment with cis-platin. In all patients, acute tubular damage was revealed by early RFP. Albumin and total protein excretion patterns suggested alterations in glomerular function. The cumulative change in RBP excretion was related to plasma creatinine concentrations following cis-platin administration. The present study demonstrates that urinary RBP is a valuable parameter for the early assessment of cis-platin-induced nephrotoxicity.
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PMID:Comparison of renal function parameters in the assessment of cis-platin induced nephrotoxicity. 791 Jun 67

A sensitive two-site enzyme immunoassay (EIA) system was established for human pS2 protein, a small estrogen-inducible secretory protein of unknown function originally identified in MCF-7 human breast cancer cells. Our EIA system is based on the sandwiching of antigen between anti-recombinant (r) pS2 antibody IgG coated on a polystyrene plate and biotinylated anti-rpS2 antibody IgG. The amount of pS2 protein was quantified by measurement of the bound enzyme activity of subsequently added streptavidin-linked beta-D-galactosidase (beta-D-galactosidase, EC 3.2.1.23). pS2 protein purified from MCF-7 culture supernatants was detectable at a concentration as low as 3 pg/ml (corresponding to 60 fg/well). This EIA system revealed that the amount of pS2-like immunoreactivity (LI) in human urine was 13.6 ng/mg creatinine (median, n = 416) and that there was no correlation between the pS2-LI concentration in urine and sex or aging. pS2-LI levels in plasma and sera of the normal subjects were 392 pg/ml (median, n = 14) and 494 pg/ml (median, n = 12), respectively. The serum level of the patients with breast cancer (528 pg/ml; median, n = 67) was not statistically different from that of normal subjects, although high levels of pS2 protein in breast cancer tissues had been reported.
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PMID:Estimation of pS2 protein level in human body fluids by a sensitive two-site enzyme immunoassay. 798 37

The effect of ceftriaxone on tobramycin-induced nephrotoxicity was investigated. Female Sprague-Dawley rats were treated during 4 and 10 days with saline (NaCl, 0.9%), ceftriaxone at a dose of 100 mg/kg of body weight/12 h subcutaneously, tobramycin at doses of 40 and 60 mg/kg/12 h intraperitoneally, or the combination ceftriaxone-tobramycin. Creatinine levels in serum were significantly higher in animals treated with tobramycin alone given at 60 mg/kg/12 h during 10 days, compared with control animals (P < 0.01) or animals receiving the combination tobramycin-ceftriaxone (P < 0.01). After 10 days of treatment, ceftriaxone did not accumulate in renal tissue but did reduce the renal intracortical accumulation of tobramycin (P < 0.05). Tobramycin given alone at either 40 or 60 mg/kg/12 h induced a significant inhibition of sphingomyelinase activity compared with control animals (P < 0.05). However, this enzyme activity was significantly less inhibited when tobramycin was injected in combination with ceftriaxone (P < 0.05). Ceftriaxone alone had no effect on the activity of this enzyme. The [3H]thymidine incorporation into the DNA of renal cortex was also significantly lower in animals treated with tobramycin-ceftriaxone compared with animals receiving tobramycin alone (P < 0.05). The 24-h urinary excretion of beta-galactosidase was significantly reduced in animals treated with the combination tobramycin-ceftriaxone compared with the administration of tobramycin alone at 40 and 60 mg/kg/12 h after 5 and 10 days (P < 0.05). Histologically, ceftriazone induced very few cellular alterations and reduced considerably the presence of typical signs of tobramycin nephrotoxicity. This investigation demonstrated that ceftriaxone protects animals against tobramycin-induced nephrotoxicity.
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PMID:Ceftriaxone protects against tobramycin nephrotoxicity. 803 Oct 41

1. Comparative studies of beta-N-acetylglucosaminidase (NAG, EC 3.2.1. 52) and beta-galactosidase (EC 3.2.1. 23) activities, protein concentration and creatinine clearance, were carried out in urine and kidney from guinea pigs treated with "toxic oil", orally administered under different conditions, related to controls. 2. Enzyme activities did not vary significantly in urine with any of the studied conditions of oil administration. By contrast, in kidney, beta-D-galactosidase disclosed a significant increase in all the treatments studied when compared to controls without treatment. 3. Urinary protein excretion, creatinine concentration and creatinine clearance were significantly greater in treated animals than in controls after 4 weeks of treatment. 4. Relative kidney weight (g/100 g body wt), was significantly lower in animals treated for 28 days with previously heated oil.
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PMID:Toxic oil syndrome: a study of renal function in guinea pigs fed toxic oil. 810 39

Creatinine concentrations and the activities of five lysosomal hydrolases were measured in the serum and urine of 14 healthy nonpregnant control women and 19 healthy pregnant women. Fractional enzyme excretion (FEE) values for beta-glucuronidase, beta-hexosaminidase, alpha-galactosidase, beta-galactosidase, and alpha-mannosidase were calculated and compared between the two groups of subjects. Fractional enzyme excretion was calculated as the ratio of enzyme clearance to creatinine clearance. The FEE values for beta-galactosidase and alpha-mannosidase between the nonpregnant and pregnant populations were not statistically different; however, relative to the nonpregnant control group, the median FEE values for beta-glucuronidase (P < 0.03), beta-hexosaminidase (P < 0.06), and alpha-galactosidase (P < 0.02) were decreased approximately 1.5-, 1.8-, and 2.7-fold, respectively, in the pregnant population. The median urinary beta-galactosidase activity for the pregnant population, when expressed on the basis of creatinine, was twofold higher than that of the control group (P < 0.0005). These data indicate that with pregnancy there are marked changes in the urinary excretion of selected lysosomal enzymes, particularly alpha-galactosidase and beta-glucuronidase. When the molecular weights of these five hydrolases were compared between kidney homogenate and control urine, a correlation of 0.96 was observed, while the correlation between control serum and control urine was 0.69. This suggests that the FEE value differences between the pregnant and control groups are most likely due to changes in tubule cell metabolism, either decreased secretion or increased reabsorption. These biochemical changes may provide a means of assessing changes in renal function during pregnancy.
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PMID:Altered urinary excretion of lysosomal hydrolases in pregnancy. 823 9


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