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)

Electron- and light microscopic analyses were conducted on leprosy skin biopsies relative to the origin of hyaluronic acid, which has previously been observed to be distributed inversely in ratio to the degree of cell- mediated immunity. The present study investigated the subcellular localization of hyaluronic acid and its degrading enzyme in various types of leprosy. Hyaluronic acid in some lepromatous leprosy cases was shown to be accumulated in the limiting membranes of the phagosomes of lepra cells and Myco-bacteria leprae have beta-glucuronidase which plays a role in the degradation of hyaluronic acid. Contrariwise, in tuberculoid leprosy, beta-glucuronidase was detected in the lysosomes of epithelioid cells and giant cells. This result suggests that the origin of hyaluronic acid is in histiocytes and at the same time it might suggest that M. leprae is in competition with enzymes of epithelioid cells for hyaluronic acid, whereas reduced or absent beta-glucuronidase in lepra cells enable bacilli to utilize the AMPS as a nutrient.
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PMID:Acid mucopolysaccharide metabolism in leprosy. 2. Subcellular localization of hyaluronic acid and beta-glucuronidase in leprous infiltrates suggestive of a host-Mycobacterium leprae metabolic relationship. 428 81

In 1962, when the immune complex in nephritic glomerular basement membrane (GBM) was clarified as being a type of GBM thickening, Amon and Gayer reported a different type of thickening in the rabbit administered hyaluronidase (an enzyme to degrade hyaluronic acid) and named it 'herniation' of the GBM. As we have been interested for a long time in the disappearance of normally present nonsulfated AMPS, presumably hyaluronic acid (HA), from the glomeruli in humans and experimental animals with chronic glomerulonephritis, we wanted to observe the activity of the enzyme in these conditions. Since a suitable histochemical method for the precise evaluation of hyaluronidase is unavailable, we instead chose beta-glucuronidase(beta-Gase), which is also an enzyme which degrades HA. The principal study was performed by means of light- and electron-microscopic histochemistry of chronic glomerulonephritis produced experimentally in rats and compared the obtained results to those in human chronic glomerulonephritis. The high activity of beta-Gase with a coincidental decrease of AMPS in the glomeruli was observed both in experimental and human chronic glomerulonephritis. The herniation type GBM thickening in the rat was coincidental with the enzyme localization with the disappearance of AMPS from foot processes of epithelial cells overlaying the lesion. The results might suggest the key role of beta-Gase in the deformation of GBM in chronic glomerulonephritis in general.
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PMID:Acid mucopolysaccharide and one of its glomerular degrading enzymes beta-glucuronidase in experimental and human glomerulonephritis. 617 21