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)

This paper is based on previous investigations, which had shown an evident acceleration of maturation and enzyme induction in several organs, not only in the lung, due to a pre- and postnatal application of prednisolone. Applying the same dosage we now investigated whether there is a similar effect of a short-term application of prednisolone in mesenchymal and parenchymal organs of young adult and presenile rats of the same strain (Chbb: THOM/SPF) analyzing the physiological cell regeneration (DNA concentration) as well as functional parameters of the glycosaminoglycan metabolism (e.g. the lysosomal enzymes beta-glucuronidase and beta-N-acetylglucosaminidase). The results show a significant age-dependent decrease of the DNA concentration (lung, spleen, skin, and rib cartilage), a significant age-dependent decrease of the total activity of the beta-glucuronidase (kidney, rib cartilage, and skin) or a significant age-dependent increase of this enzyme activity (spleen and liver) respectively as well as a significant decrease of the beta-N-acetylglucosaminidase activity (skin and rib cartilage) or a significant increase of this enzyme activity (spleen and lung). After application of prednisolone the rats showed a significant reduction of the DNA concentration only in the skin of young adult rats, but no changes in the other organs of the young adult or presenile animals compared to untreated controls. Similar to our findings after postnatal prednisolone application, we found the greatest increases or decreases respectively of the activities of these lysosomal enzymes due to 2- to 3-fold or 4- to 5-fold prednisolone application. Again similar to our previous findings, we found the phenomena of adaptation and rebound effects including the so-called over-compensation in the young adult and especially in the presenile rats but these effects were delayed and weaker in most of the older animals compared to the young adult rats.
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PMID:[Age-related changes in cell content (DNA) and glycosaminoglycan-degrading enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase of connective tissue and parenchymal organs of the rat caused by 6-methylprednisolone (enzyme induction, adaptation, acceleration of maturation and possible modification of aging]. 376 77

Quantitative biochemical analyses of the beta-glucuronidase total activity and the total DNA-content carried out on selected parenchymal and mesenchymal organs of 455 Wistar inbred rats (strain Chbb:THOM (SPF) from 56 litters (untreated or treated with 1 mg betamethasone/kg b.w. s.c. on both the 18th and 19th days of pregnancy, applied to the mother animal) led to the following results: The DNA-content of lung, liver, kidney, skin and rib cartilage declined continuously both in the controls and in the treated group during the postnatal observation period (from the 1st to the 15th day p.p.). The prenatal glucocorticoid administration led to a decline in the DNA-content in comparison to the untreated controls, especially evident in the first postnatal days. The beta-glucuronidase activity of lung, liver and kidney showed an increase in the postnatal development phase to a maximum occurring organ-dependently on different days with a decrease afterwards. Due to glucocorticoid-pretreatment of the mother animals the newborn rats showed significantly higher enzyme values within the first postnatal days than did the untreated controls. Between the 6th and 9th day (depending on the organ) the same beta-glucuronidase activities could be found on pretreated and untreated animals. For the further ages tested in this study (till the 15th day of postnatal development) the enzyme activity of the experimentally treated litters was lower than that of the untreated controls. In connection with related findings, especially regarding morphological changes in the lung, the induction of beta-glucuronidase as well as the decrease in the DNA-content due to prenatal glucocorticoid pretreatment are discussed in terms of a maturation acceleration.
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PMID:[Changes in total beta-glucuronidase activity and DNA content of various tissues and organs of newborn rats after prenatal administration of glucocorticoid]. 719 90

Not only in the experimental leprosy, primary aim to make every experimental model crucial for the medical research has been the simulation of the aspect of disease encountered in human case by the simplest possible way. The present study was conducted to do so making some variations in addition to the experimental lepromata, produced in nude mice by Sasaki et al. and by Hamit, utilizing a leproma-derived and cultivated Mycobacterium HI-75 (HI-75). In this study HI-75, Mycobacterium bovip BCG (BCG) and female SPF ddY(ddY) were utilized to make experimental models. In addition to these combinations, the effect of the immunization of beta-glucuronidase binding protein (BGBP) to the lesion was also examined. The BGBP extracted from pisum sativum and utilized in this study shows cross-immunoreactivity with those of HI-75 and M. leprae. As the results, the lesions caused by HI-75 and BCG were somewhat resembling though HI-75 caused a little more extensive lesions especially in lymphocytic and monocytic infiltration. Also HI-75 caused distinct nerve lesions(NL) in which the bacilli were often encountered in the endoneurium but not in those by BCG. Contrarily in mice immunized with BGBP, the lesions were only a little milder and the affected tissue was a little fibrosed. However, in NL the solid form HI-75 were more often observed in the endoneurium. The results indicated that the effect of BGBP immunization on the HI-75 induced lesion was not very clear by the present study alone, however, the proposed models itself should be and will become very useful, for experimental leprology with only slight modifications.
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PMID:[On the lesions caused by a leproma-derived and cultivated Mycobacterium HI-75 produced in ddY mice. With special reference to a factor influencing the lesions and the differences from those by BCG]. 951 47