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 rats with induced syndrome of chronic magnesium deficiency, occurrence of haemolytic anaemia in conjuction with a shortening of the erythrocyte survival time and marked reticulocytosis among other symptoms became noticeable. In the present experiment the authors undertook to study the behaviour of the lysosomal enzymes in the erythrocytes of magnesium-deficient rats. In these animals anaemia and reticulocytosis as well as a marked increase in the percentage of the erythrocytes showing positive reactions to the acid phosphatase and beta-glucuronidase tests developed. It seems likely that the positive lysosomal reactions were obtained with younger blood cells which did not stain with brilliant cresyl blue but still retained single lysosomes in their cytoplasm. This assumption was confirmed by ultrastructural studies which demonstrated the presence of siderosomes inside both the reticulocytes and the mature erythrocytes. The changes in the percentages of reticulocytes and enzyme-positive erythrocytes were independent of the histological structure of the experimental rat's thymus. In the reticulocytes as well as in the mature erythrocytes, the noteworthy presence of degenerated mitochondria containing electron-dense material seems to be a morphological sign of impairment of the magnesium-deficient rat's erythrocytes.
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PMID:The activity of certain hydrolases of rat erythrocytes in experimental magnesium deficiency. 99 1

The effects of a toxic dose of Mycoplasma fermentans on levels of lysosomal enzymes in mice were examined. Washed cell suspensions (approximately 10(10) colony-forming units) of a recent isolate of M. fermentans were injected intraperitoneally into 3- to 4-week-old BALB mice, and levels of acid phosphatase and beta-glucuronidase were monitored in liver, spleen, thymus, and serum. Levels of acid phosphatase remained essentially normal, but levels of beta-glucuronidase were markedly evevated in serum and to a lesser extent in liver and thymus. The peak response of serum beta-glucuronidase was noted at 8 h postinjection, with a level of 30 mug of phenolphthalein released per ml per h, representing a six-fold increase over control levels. Pretreatment with BCG did not potentiate the effect as it did with endotoxin. The implication of this increased lysosomal enzyme activity in "lethal toxicity" is that that the increase may be secondary to some other cytotoxic event, or that the affinity of mycoplasmas for biological membranes may be involved. The data suggest that the role of lysosomal enzymes in other models of mycoplasma-induced disease should be evaluated.
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PMID:Levels of lysosomal enzymes in tissues of mice infected with Mycoplasma fermentans. 109 4

The radioactivity level in blood, bile, urine and contents of parts of the gastro-intestinal tract in rats was studied after subcutaneous administration of 3-H-1,2-dimethylhydrazine (3-H-SDMH) which induces colonic tumours. The alkylation of DNA, RNA and protein in the intestinal mucosa, liver and kidneys was estimated 1 h to 28 days after 3-H-SDMH treatment from the 3-H-incorporation into these macromolecules. Administration of 3-H-1,2-diethylhydrazine (3-H-SDEH) which does not induce intestinal tumours was made as a control. Fifteen to 30 min after 3-H-SDMH treatment, marked radioactivity was found in blood, bile, urine and in contents of all regions of gastro-intestinal tract. After 3-H-SDMH administration no label occurred in the contents of localized segments of gastro-intestinal tract although it was present in blood, bile and urine. 3-H-SDMH methylated DNA, RNA and proteins of intestinal mucosa, liver and kidney to a high degree. One hour after 3-H-SDMH treatment the incorporation of label into protein of intestinal mucosa was higher than into liver and kidneys. 3-H-SDEH did not alkylate macromolecules in these organs but did so in thymus, spleen and brain, which are target organs for this carcinogen. After total hepatectomy, 3-H-SDMH did not methylate macromolecules of the intestinal mucosa. The following mechanism for the carcinogenic effect of SDMH is suggested. A carcinogenic metabolite of SDMH forms, in the liver, a conjugate with glucuronic acid. This glucuronide enters the gut both with bile and directly via the circulation. Microbial beta-glucuronidase releases the active metabolite which, in turn, alkylates tissue macromolecules.
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PMID:The mechanism of carcinogenic action of 1,2-dimethylhydrazine (SDMH) in rats. 114 Aug 67

General and histochemical observations of the thymus were carried out in guinea pigs after injection of cyclophosphamide (280 mg/kg). Acute involution of the thymus induced by cyclophosphamide was accompanied by marked enlargement of Hassall's corpuscles in the first week after injection. However, the markedly enlarged Hassall's corpuscles disappeared entirely by the fourth week. Large cells characterized by pale nuclei with one or two prominent nucleoli became aggregated in the enlarged Hassall's corpuscles by the second week. Their cytoplasm frequently was foamy or vesicular in appearance. Histochemical observations revealed strong activities of nonspecific esterase, acid phosphatase and beta-glucuronidase in these cells. Staining for these lysosomal hydrolytic enzymes was evident not only intracellularly but also extracellularly, indicating the dissolution of Hassall's corpuscles by intensive extracellular enzyme release.
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PMID:Clastic cells of Hassall's corpuscles during acute involution of the thymus induced by cyclophosphamide in guinea pigs. 179 68

Mature and immature male rabbits were fed for 120 and 20 days, respectively, a commercial diet containing theobromine in amounts of 0, 0.5, 1 and 1.5 per cent. Clinical, haematological, histopathological and histoenzymological examinations were performed. Mortality, which appeared dose- and time-related, was severe and rapid, mostly in the 1 and 1.5 per cent groups and was attributed to cardiac failure. Theobromine administration resulted in marked changes in thymus and testes and the severity of lesions appeared to be related to the amounts of the ingested methylxanthine. The earliest thymic alterations in immature rabbits consisted of a blurring of demarcation between cortex and medulla accompanied, in the more advanced stages, by a decreased lymphocyte density. Similar lesions were observed in mature animals which had died in the earlier phase of the study. Testicular alterations ranged from vacuolation of spermatids and spermatocytes to multinucleated cell formation and oligospermia or aspermia with extensive degeneration of tubule cells. Some necrotic and post-necrotic myocardial foci were also recorded. The increase in testicular activity of beta-glucuronidase in immature rabbits compared to the untreated animals provided further evidence of an early theobromine-induced damage of the testes.
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PMID:Toxic effects of theobromine on mature and immature male rabbits. 291 9

Thymocytes, bone marrow lymphocytes, as well as lymphocytes from spleen, lymphoid nodes and peripheral blood were obtained from BALB/c mice. Subpopulations of BALB/c bone marrow T-lymphocyte precursors and immature (small) and mature (large) thymocytes, as established by the percentage of terminal deoxynucleotidyl transferase (TdT) and peanut agglutinin (PNA) positive cells, were obtained by centrifugation on discontinuous density gradients. The activities of N-acetyl-beta-glucosaminidase (NAG), beta-glucuronidase (BG), acid alpha-naphthyl acetate esterase (ANAE) and alpha-naphthyl acetate esterase (NAE) were determined by enzymatic assays of cell extracts of the diverse T-lymphocyte subpopulations, in order to follow their evolution with the maturation of the T-lymphocytes in the thymus. These activities were compared with that determined in lymphocytes from spleen, lymphoid nodes and peripheral blood. The glucidases BG and NAG and the esterases ANAE and NAE present a high decrease in their activities from bone marrow T-lymphocyte progenitors to immature thymocytes. BG, NAG and ANAE activities undergo an about 3-fold increase with the evolution of the thymocytes from small to large cells. Whereas the level of the NAE activity decreases (2-fold) with that evolution of the thymocytes. Lymphocytes from spleen and lymphoid nodes exhibit activities of the glucidases and, specially, the esterases marked by higher than those of thymocyte populations. Peripheral blood lymphocytes also present NAG, ANAE and NAE activities higher than in thymocytes, but their BG activity is lower.
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PMID:The distribution of N-acetyl-beta-glucosaminidase, beta-glucuronidase, acid alpha-naphthyl acetate esterase and alpha-naphthyl acetate esterase in subpopulations of thymocytes, bone marrow cells and other lymphoid organs in mice. 293 37

Delayed toxicity of a single dose of 300 mg/kg cyclophosphamide (CP) was investigated in female DBA/2 mice. Lethality was low up to 30 days but increased markedly afterwards reaching a peak of 50% between 50-70 days with a total mortality of more than 80% by day 120 after CP. One week before death, the mice suffered a sharp loss of weight and showed typical signs of wasting disease. There was a decrease in the white cell count and lymphocyte neutrophil ratio was reversed as a result of lymphocyte depletion whereas neutrophil count remained similar to the controls. Profound lymphocyte depletion was also observed in light and electron microscopy preparations of thymus from mice with CP-induced wasting disease. Histochemical methods demonstrated increased activity of four lysosomal enzymes, acid phosphatase, beta-glucuronidase, E600 resistant esterase and n-acetyl-beta-glucosaminidase, in the thymus of treated mice. Acid phosphatase was notably active in thymus epithelial cells; the reaction product was localized in multiple primary Golgi lysosomes, Golgi cisternae, cisternae of the endoplasmic reticulum, and secondary lysosomes. The appearance of numerous cystic formations, as well as the activation of the lysosomal system and the presence of large areas of degradation support the assumption that CP-delayed toxicity is accompanied by thymus involution. Delayed mortality was partially prevented when syngenic bone marrow cells were injected as early as 24 h after CP injection. On the other hand thymus transplants were incapable of reducing delayed lethality. It is suggested that CP provokes a delayed wasting syndrome with thymic involution that is not caused by a direct effect on specific thymus structures but rather secondary to a primary injury to pre T cells in bone marrow.
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PMID:Delayed toxicity of cyclophosphamide in normal mice. 355 94

Human thymuses, ranging in age from newborn to 62 years old, were studied enzyme histochemically. The thymic epithelial cells covering cortical surface and bordering vascular areas in the medulla were positive for 5'-nucleotidase, but not for other enzymes. The thymic epithelial cells composing Hassall's corpuscles were positive for acid phosphatase, esterases, beta-glucuronidase, and alkaline phosphatase, regardless of age, but totally negative for 5'-nucleotidase and ATPase. All enzymes examined except for beta-glucuronidase were demonstrated in some of the thymic epithelial cells scattered in the medulla, although the pattern of distribution and the degree of positivity were different by enzymes. These findings suggest that the thymic epithelial cells are composed of functionally heterogenous subpopulations. Acid phosphatase was demonstrated in thymocytes in both cortex and medulla, but 5'-nucleotidase and ATPase were observed in some thymocytes in the medulla of young thymus.
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PMID:Enzyme histochemical study on human thymus and its age change. 630 84

We have examined a human thymoma, round-oval epithelial-type cell with moderate lymphocytic infiltration, whose major lymphocytic component (67%), unlike the minor one (33%), did not form rosettes with sheep red blood cells (E rosettes). However, these cells were of T-cell nature as indicated by the positive staining for both acid phosphatase and beta-glucuronidase, two well-accepted cytochemical markers for T cells. The non-E-rosetting lymphocytes expressed T 10, but not T 3 and T 6 antigens. Moreover, they lacked both peanut agglutinin and Fc-IgG receptors. On the contrary, 71 and 19% of the E-rosetting cells were PNA- and Fc-IgM-receptor positive, respectively. Furthermore, the non-E-rosetting cells were phytohemagglutinin unresponsive. The non-E-rosetting lymphocytes were larger (greater than 7 micron) than the E-rosetting cells and showed a different nuclear chromatin pattern. These immunological, cytochemical, and morphological features strikingly resemble those exhibited by cells (prothymocytes) normally found only in fetal thymus. On the basis of these findings we hypothesize the existence in this thymoma of a prothymocyte-like infiltration.
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PMID:A human thymoma with prothymocyte-like infiltration. 660 37

A number of cell surface markers (T200, ThB, Thy1, Lyt1 and Lyt2 and a glycolipid) and enzymes (ATP-ase, acid phosphatase, beta-glucuronidase, 5'-nucleotidase, non-specific esterase, ANAE and chloroacetate esterase) were determined for two murine T-cell lymphomas: the DBA/2-strain-derived SL2 with a phenotype close to that of a mature thymocyte and the GRS-strain-derived GSRL13 with a phenotype of a more primitive thymocyte. While the pattern of expression of the enzymes was similar for SL2 and GRSL13 and as such indistinguishable from that of the majority of thymus cells, the pattern of cell surface antigen expression was clearly different. GRSL12 cells express the ThB antigen and a glycolipid antigen detectable with monoclonal antibody 30-H11, but not Lyt1 and Lyt2 antigens. SL2 cells, however, do not express ThB and the glycolipid antigen, but do express Lyt1 and Lyt2.
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PMID:Cell surface antigen phenotypes and enzyme expression patterns of two murine T-cell lymphomas derived from early and/or mature thymus cells. 698 39


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