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:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although early studies in germ-free rats showed almost complete dependence on dimethylhydrazine (DMH) colon carcinogenesis upon the presence of colon bacteria, no adequate explanation was given for the 20% tumor incidence observed in germ-free animals. Bacterial activation of liver microsomal products releasing active proximate carcinogens has been the accepted reason for the exquisite specificity DMH has for the colon. Recent work, including the present study, show the colon mucosa is capable of metabolizing carcinogens and activating conjugating forms metabolized in the liver independent of the intestinal microflora. Mucosal beta-glucuronidase production was assayed in coded, scraped mucosa samples from the duodenum/jejunum, ileum, right colon, and left colon of normal and DMH-treated rats. Normal mucosal beta-glucuronidase production was highest in the left colon followed by the right colon, duodenum, and ileum, respectively. Enzyme production in the left colon was significantly increased 24 hours after injection of 25 mg/kg body weight DMH. No elevation was seen in other mucosal samples. Metabolism of DMH to oxidated forms conjugated to glucuronic acid is well established. Thus, this study offers a possible role for carcinogen, induction of a metabolic enzyme in its target tissue.
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PMID:Induction of colon mucosal beta-glucuronidase production as a mechanism for 1,2-dimethylhydrazine colon carcinogenesis. 663 8

beta-Glucuronidase activity increased in the serum of BALB/c mice during the growth of the IgM-secreting plasmacytoma, TEPC-183. The increase appeared to correlate with tumor burden. The beta-glucuronidase activity in tissue homogenates of spleen, liver, and kidney from tumor-bearing mice also increased significantly compared to the levels found in corresponding tissues from normal control mice. Assays of lysosomal and microsomal fractions from livers of TEPC-bearing mice indicated that approximately 70% of the enzyme activity was associated with the lysosomal fraction and the remainder with the microsomal fraction. A similar distribution was found in homogenates prepared from the plasmacytoma itself. In contrast to this the beta-glucuronidase activity in livers from normal BALB/c mice is nearly equally distributed between lysosomal and microsomal fractions.
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PMID:The effect of TEPC-183 plasmacytoma growth on beta-glucuronidase activity in serum and tissues of tumor-bearing mice. 665 89

The incidence, distribution, size, and histopathology of rat small and large bowel tumors induced by sequential administration of 1,2-dimethylhydrazine followed by cecal placement of one of six differing types of suture materials were systematically examined. In addition, measurements of beta-glucuronidase activities in large bowel contents followed by fecal trace metal determinations were done. The results indicate that specific slowly absorbed and nonabsorbable suture materials in the absence of a surgical anastomosis promote tumor induction locally in the rat cecum. In addition, cecal suture material composed of multifilament stainless steel wire enhanced tumor development at a "downstream" site in the distal colon, paralleling increased fecal beta-glucuronidase activities at this site and implicating a possible luminally mediated mechanism for colon tumor development in this animal model.
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PMID:Differential effects of surgical suture materials in 1,2-dimethylhydrazine-induced rat intestinal neoplasia. 672 11

The specific activities of five glycohydrolases of lysosomal origin (beta-N-acetylglucosaminidase, beta-glucuronidase, beta-galactosidase, alpha-mannosidase and alpha-fucosidase) were measured in different types of primary and metastatic tumors of the human nervous system. The activities of these hydrolytic enzymes in samples of tumor tissue were compared with those in the white matter of 'control' tissue. The specific activities of beta-glucuronidase and beta-N-acetylglucosaminidase were significantly higher (P less than 0.001) in each group of tumors than in normal cerebral matter. The activities of the other hydrolases were sometimes significantly increased in primary tumors, but not always. In metastatic tumors, they were also significantly higher (P less than 0.01).
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PMID:Study of some lysosomal glycohydrolases in tumors of the nervous system. 672 45

Sprague-Dawley rats bearing 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumors were treated with either of two aromatic alkylating agents, aniline mustard or melphalan, alone or combined with ovariectomy. Both drugs were applied once a week for 8 weeks. Eight-four percent of the tumors responded to ovariectomy, 38% regressing completely and 46% regressing partially. Aniline mustard, though virtually ineffective as a single agent, appeared synergistic with ovariectomy: a 100% regression rate (72% complete, 28% partial) was observed for this combination. Treatment with melphalan was as effective as ovariectomy, but the combination of melphalan with ovariectomy was no more effective than either treatment alone. The end product of aniline mustard metabolism, p-hydroxyaniline mustard O-glucuronide, may be more extensively activated by beta-glucuronidase in hormonally regressing than in growing or stationary tumors. Intratumoral levels of beta-glucoronidase occurring in DMBA-induced tumors 4 days after ovariectomy were found to be similar to those in the aniline mustard-sensitive mouse plasma cell tumor ADJ/PC6. It remains to be more extensively studied whether an effect of endocrine treatment on tumor beta-glucuronidase levels, and possibly on intracellular distribution of enzyme, could be used therapeutically. An effectively scheduled cytostatic treatment (with a drug conjugate such as that formed metabolically from aniline mustard) in conjunction with ovariectomy might be effective in the treatment of hormone-responsive breast cancer.
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PMID:Enhanced cytostatic effectiveness of aniline mustard against 7,12-dimethylbenz[a]anthracene-induced rat mammary tumors during regression in response to ovariectomy. 678 69

The incidence, distribution, size, and histopathology of rat small and large bowel tumors induced by sequential administration of 1,2-dimethylhydrazine followed by either small bowel resection, 50% jejunoileal resection, or 50% jejunoileal bypass were examined in addition to measurements of transit times and beta-glucuronidase activities in large bowel contents. The results indicate that even limited small bowel resection or bypass promotes intestinal neoplasia, particularly in the large bowel, and this effect seems independent of the chronic injury imposed by suture lines. Although no differences in transit times were observed, increased beta-glucuronidase activities in both cecum and distal colon of resected but not bypassed rats was detected. Moreover, an apparent subsite redistribution of small bowel tumors to ileum and large bowel tumors to more proximal colon in bypassed rats suggests that the mechanisms involved for tumor enhancement differ substantially from those in resected rats.
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PMID:Effects of small bowel transection, resection, or bypass in 1,2-dimethylhydrazine-induced rat intestinal neoplasia. 682 83

The lysosomal response of a murine macrophage-like tumor cell line (J774) during persistent infection with Coxiella burnettii was examined. By using acid phosphatase as a lysosomal marker, it was shown that phagosome-lysosome fusion occurred in J774 cells persistently infected with C. burnetii. This observation was verified using thorium dioxide, an electron-dense compound that is sequestered in secondary lysosomes. The phagolysosomes contained viable replicating rickettsiae. Spectrofluorometric analysis indicated that the phagolysosomal pH of persistently infected cells was acidic. In attempts to correlate rickettsial survival with lysosome function, the activities of several lysosomal enzymes were assayed in both infected and uninfected cells. Activities of acid phosphatase and beta-acetylglucosaminidase were not significantly altered during infection. However, infected cells appeared to display slightly higher intracellular lysozyme, beta-glucuronidase, and beta-galactosidase activities.
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PMID:Lysosomal response of a murine macrophage-like cell line persistently infected with Coxiella burnetii. 685 16

The clinical findings and response to treatment of leptomeningeal metastases from solid tumors are analyzed in 90 patients treated at Memorial Sloan-Kettering Cancer Center during the period from January 1975 to February 1980. Patients included those who had either typical clinical findings of leptomeningeal tumor or conclusive laboratory evidence supporting the diagnosis. Carcinoma of the breast (46 patients), lung (23 patients) and melanoma (11 patients) were the common primary tumors. Symptoms of leptomeningeal metastasis occurred as the presenting sign in five patients and as late as ten years after the primary tumor was diagnosed in four other patients. Most patients had active systemic disease outside the nervous system. Signs and symptoms could be classified as involving either the brain, cranial nerves, or spinal nerves. Most patients had either symptoms or signs in more than one area at the time the diagnosis was established. The initial spinal fluid examination was abnormal in all but three patients, but only 49 had cytologic evidence of leptomeningeal metastases. Repeated spinal fluid assay yielded a positive cytology in 82 patients. Measurement of biochemical markers, including beta-glucuronidase, carcinoembryonic antigen and lactic dehydrogenase, assisted in the diagnosis. Approximately half of the patients treated by intraventricular methotrexate experienced improvement or stabilization of neurological symptoms for more than a month; median survival was 5.8 months after diagnosis, with a range of 1--29 months. In 18 patients disease was limited to the nervous system, and median survival was eight months, with four patients surviving one year and two patients for two years. Side effects of therapy were, for the most part, minor. We conclude that vigorous treatment of leptomeningeal metastases with intrathecal chemotherapeutic agents improves symptomatology in some patients, and at times prolongs survival.
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PMID:Diagnosis and treatment of leptomeningeal metastases from solid tumors: experience with 90 patients. 689 13

The control of differentiation by tumor-promoting phorbol diesters including 12-O-tetradecanoylphorbol-13-acetate (TPA) was investigated using cells from human myeloid leukemia lines and sublines that were blocked at different stages of maturation. The myeloid leukemia cells that were blocked at the myeloblast-promyelocyte stage of maturation (KG-1, HL-60, and ML-3) had a prominent response when cultured with TPA. The cells became adherent, developed pseudopodia, displayed macrophage characteristics by light microscopy, developed nonspecific acid esterase activity, phagocytized yeast, slightly reduced nitro blue tetrazolium, displayed Fc-immunoglobulin G receptors, and killed bacteria. Lysozyme secretion and enzyme activity for beta-glucuronidase and acid phosphatase increased 2- to 20-fold concomitant with macrophage differentiation. The myeloid leukemia cells that were blocked at the undifferentiated myeloid blast stage of maturation (KG-1a and K562) were completely resistant to TPA-induced macrophage differentiation. We examined ten macrophage functions in the myeloid cell lines and sublines after exposure to phorbol diesters. The leukemic lines blocked at the myeloblast-promyelocyte stage of maturation expressed almost all the macrophage-specific functions. Phorbol diesters probably induced differentiation through a common cellular mechanism because the macrophage-differentiated events could not be dissociated. In sharp contrast, the early myeloid blast cells (KG-1a and K562) were incapable of acquiring any of the macrophage-specific functions after exposure to phorbol diesters. The KG-1a variant, in particular, should provide a good model to help elucidate the regulatory mechanism controlling the expression of macrophage functions during exposure to phorbol diesters.
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PMID:Phorbol ester effect on differentiation of human myeloid leukemia cell lines blocked at different stages of maturation. 693 77

The present study sought to delineate the phenotypic heterogeneity of the human T-cell malignancies. Twenty T-cell neoplasms were investigated for reactivity with the OKT hybridoma monoclonal antibodies and expression of acid alpha-naphthyl acetate esterase (ANAE), beta-glucuronidase (BG), and acid phosphatase (AP) activity. Twelve cases (Mycosis fungoides, Sezary syndrome, cutaneous T-cell lymphoma, chronic lymphocytic leukemia) were OKT3'T4', ie, expressed the phenotype commonly associated with mature T-helper cells. These cases were further divisible into ANAE+BG+ (6 cases), ANAE-BG+ (5 cases), and ANAE-BG- (1 case) phenotypes. In contrast to the 12 OKT3+T4+ cases, the remaining 8 cases showed considerable inter- and intratumor heterogeneity with respect to reactivity with the OKT antibodies. Six of these cases (acute lymphoblastic leukemia, lymphoblastic lymphoma) expressed phenotypes consistent with various intrathymic stages of T-cell differentiation. Five of the latter 6 cases were AP+BG+ANAE-, analogous to the majority of normal cortical thymocytes; an OKT3+T4-T8+T10+ neoplasm was ANAE+, analogous to normal medullary thymocytes. Two cases expressed the previously undescribed OKT3+T4-T8-T10+ phenotype. These studies demonstrate that the T-cell malignancies are divisible into phenotypes which correspond to normal maturational stages of T-cell differentiation and functionally distinct T-cell subsets. Phenotypic analysis of the human T-cell malignancies may provide a basis for understanding their biological heterogeneity and may aid in the identification of transitional stages of T-cell differentiation and minor T-cell subsets.
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PMID:Phenotypic heterogeneity of human T-cell malignancies: demonstration by monoclonal antibodies and cytochemical markers. 697 45


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