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Hexb  -  hexosaminidase B

Rattus norvegicus

Synonyms: Beta-N-acetylhexosaminidase subunit beta, Beta-hexosaminidase subunit beta, Hexosaminidase subunit B, N-acetyl-beta-glucosaminidase subunit beta
 
 
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Disease relevance of Hexb

  • High dietary iron resulted in greater sensitivity to GM (100 mg/kg body wt) toxicity in terms of elevated urinary excretion of n-acetyl-beta-glucosaminidase (NAG) and increased mineralization, casts and megalocytes in renal tubules [1].
  • Associated with hyperoxaluria was an increase in urinary levels of renal enzymes, gamma-glutamyl transpeptidase, N-acetyl-beta-glucosaminidase, and alkaline phosphatase [2].
  • Urinary excretion of gamma-glutamyl transpeptidase, angiotensin I converting enzyme, beta-galactosidase and N-acetyl-beta-glucosaminidase was evaluated in 30 patients with idiopathic calcium oxalate urolithiasis [3].
  • DMS failed to prevent renal toxicity as indicated by weight loss, serum creatinine concentration, renal histology, and the urinary excretion of N-acetyl-beta-glucosaminidase, a renal tubular enzyme [4].
  • Ischemia and revascularization alone caused increased mucosal permeability to sodium fluorescein, increased N-acetyl-beta-glucosaminidase release from the mucosa into the lumen, increased malondialdehyde content in the mucosa, and increased myeloperoxidase activity in the mucosa [5].
 

High impact information on Hexb

  • DNA, cytochrome c oxidase, glucose-6-phosphatase, and N-acetyl-beta-glucosaminidase content in hepatic plasma membrane preparations were not substantially different in diabetic as compared with control animals [6].
  • Changes in biliary excretion of lysosomal enzymes accompanying chloroquine and glucagon administration were associated with morphologic evidence of autophagy as assessed by electron microscopy and by increased fragility of hepatic lysosomes as assessed by latency of N-acetyl-beta-glucosaminidase [7].
  • Both chloroquine and glucagon immediately caused a marked and parallel decrease in biliary excretion of three lysosomal enzymes, N-acetyl-beta-glucosaminidase, beta-glucuronidase, and beta-galactosidase, to 25%-30% of baseline values (p less than 0.01) [7].
  • After monensin treatment, the median density of both galactosyl transferase and 5'-nucleotidase increased from 1.128 to 1.148, and the median density of both N-acetyl-beta-glucosaminidase and horseradish peroxidase taken up by endocytosis decreased from 1.194 to 1.160 [8].
  • Enrichment of acid hydrolase activities (aryl sulfatase, N-acetyl-beta-glucosaminidase, tartrate-sensitive acid phosphatase, and cholesteryl ester acid hydrolase) and cathepsin D mass was also comparable in early and late endosomes but was considerably lower in the receptor-recycling fraction [9].
 

Chemical compound and disease context of Hexb

 

Biological context of Hexb

  • In vehicle-treated DOCA-salt rats, renal blood flow and creatinine clearance decreased, and urinary excretion of protein, blood urea nitrogen, fractional excretion of sodium, and urinary N-acetyl-beta-glucosaminidase activity increased [15].
  • Hormonal regulation of isoenzymes of N-acetyl-beta-glucosaminidase and beta-galactosidase during spermatogenesis in the rat [16].
  • There were no significant changes in the time course of systolic blood pressure, heart rate, urine volume, or urinary sodium, protein and N-acetyl-beta-glucosaminidase (NAG) excretion between the two groups [17].
  • The enzyme is identified as N-acetyl-beta-glucosaminidase (NA beta G) on the basis of substrate specificity and susceptibility to inhibition by N-acetylgalactosamine [18].
  • We identified the cellular sites of glycosaminoglycan hydrolysis by localizing a key enzyme, N-acetyl-beta-glucosaminidase, in the rat periodonatal ligament [19].
 

Anatomical context of Hexb

  • We also examined the morphology of the ileal mucosa after deposition of LPC in the gut lumen, and determined N-acetyl-beta-glucosaminidase, 5'-nucleotidase, and alkaline phosphatase activities in suspensions of isolated mucosal cells and different concentrations of LPC [20].
  • The specific activities of isoenzymes I and II of N-acetyl-beta-glucosaminidase increased markedly in association with the formation of spermatogonia and spermatocytes, and then declined with the appearance of spermatids [16].
  • Isoenzymes of beta-galactosidase and of N-acetyl-beta-glucosaminidase were assayed during development of rat testis and as a function of hormonal treatments [16].
  • Formation of the acrosome in developing spermatids is associated with the induction of new forms of beta-galactosidase (isoenzyme II) and N-acetyl-beta-glucosaminidase (sperm isoenzyme) [16].
  • Rats injected with mercuric chloride exhibited a phospholipiduria associated with sharp increases (7- to 15-fold) in the urinary excretion of brush border membrane enzymes, whereas N-acetyl-beta-glucosaminidase increased less than 3-fold [21].
 

Associations of Hexb with chemical compounds

  • In the absence of inhibitor, ischaemia and revascularisation caused increased mucosal permeability to sodium fluorescein, increased N-acetyl-beta-glucosaminidase release from the mucosa into the lumen, increased malondialdehyde content in the mucosa and increased myeloperoxidase activity in the mucosa [22].
  • Feeding sodium deoxycholate orally to rats for four days caused depression of the activity of the small intestinal enzymes lactase, sucrase, maltase, alkaline phosphatase, and N-acetyl-beta-glucosaminidase [23].
  • BN 52021, a specific platelet activating factor antagonist, did not influence the myeloperoxidase activity, but it decreased the formation of malondialdehyde and the increases in mucosal permeability and N-acetyl-beta-glucosaminidase release, although not to the same extent as quinacrine and NDGA [22].
  • Bile acids, cholesterol, and phospholipid were measured in bile, and three lysosomal glycosidases (beta-glucuronidase, beta-galactosidase, and N-acetyl-beta-glucosaminidase) and total protein were measured in bile and liver [24].
  • The increase in 3H-thymidine incorporation induced by hexosaminidase B was also inhibited by mannan and PIA [25].
 

Other interactions of Hexb

  • To analyze transcription levels of Hex alpha and beta subunits (Hexa and Hexb, respectively), real-time relative quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis was performed using the LightCycler system [26].
  • In aberrant crypts, both Hexa and Hexb were significantly down-regulated to 0.266 (P < 0.002) and 0.131 (P < 0.001) units, respectively, compared with those in morphologically normal crypts, with beta-actin as the internal standard [26].
 

Analytical, diagnostic and therapeutic context of Hexb

  • Two proteins were resolved by gel filtration to be in supernate: n-acetyl-beta-glucosaminidase and a filamentous protein which attaches n-acetylglucosaminidase to the membrane surface thereby providing bidirectionality to the array of enzyme [27].
  • Analytical cell fractionation of freshly isolated ATII cells confirmed that lgp-120 was only present in structures containing the lysosomal matrix enzyme N-acetyl-beta-glucosaminidase [28].
  • Following hypophysectomy of rats at 26 days of age or in adulthood the specific activities of the lysosomal enzymes beta-galactosidase I and N-acetyl-beta-glucosaminidase I and II increased markedly, while the acrosomal beta-galactosidase II was undetectable [16].
  • It was demonstrated that upon Percoll density gradient centrifugation the enzyme from this tissue distributed parallel to the lysosomal marker enzymes beta-N-acetylhexosaminidase and beta-galactosidase, indicating a lysosomal localization for this enzyme [29].
  • The localization and activity of the lysosomal enzyme, N-acetyl-beta-glucosaminidase, has been studied in unfixed frozen sections of tissues from normal and hemorrhaged rats with the use of a modified postcoupling technique [30].

References

  1. Iron supplementation increases gentamicin nephrotoxicity in rats. Kays, S.E., Crowell, W.A., Johnson, M.A. J. Nutr. (1991) [Pubmed]
  2. Urinary enzymes and calcium oxalate urolithiasis. Khan, S.R., Shevock, P.N., Hackett, R.L. J. Urol. (1989) [Pubmed]
  3. Increased urinary excretion of renal enzymes in idiopathic calcium oxalate nephrolithiasis. Baggio, B., Gambaro, G., Ossi, E., Favaro, S., Borsatti, A. J. Urol. (1983) [Pubmed]
  4. The effect of heavy metal chelators on the renal accumulation of platinum after cis-dichlorodiammineplatinum II administration to the rat. Graziano, J., Jones, B., Pisciotto, P. Br. J. Pharmacol. (1981) [Pubmed]
  5. Oxygen radicals, lipid peroxidation, and neutrophil infiltration after small-intestinal ischemia and reperfusion. Otamiri, T. Surgery (1989) [Pubmed]
  6. Glucagon-stimulable adenylyl cyclase in rat liver. The impact of streptozotocin-induced diabetes mellitus. Dighe, R.R., Rojas, F.J., Birnbaumer, L., Garber, A.J. J. Clin. Invest. (1984) [Pubmed]
  7. Pharmacologic perturbation of rat liver lysosomes: effects on release of lysosomal enzymes and of lipids into bile. Sewell, R.B., Grinpukel, S.A., Zinsmeister, A.R., LaRusso, N.F. Gastroenterology (1988) [Pubmed]
  8. Inhibition of pinocytosis in rat embryo fibroblasts treated with monensin. Wilcox, D.K., Kitson, R.P., Widnell, C.C. J. Cell Biol. (1982) [Pubmed]
  9. Acid hydrolases in early and late endosome fractions from rat liver. Runquist, E.A., Havel, R.J. J. Biol. Chem. (1991) [Pubmed]
  10. Studies of monokines as mediators of the acute phase response: effects on sialyltransferase, albumin, alpha 1-acid glycoprotein and beta-N-acetylhexosaminidase. Woloski, B.M., Gospodarek, E., Jamieson, J.C. Biochem. Biophys. Res. Commun. (1985) [Pubmed]
  11. Phospholipase C-mediated intestinal mucosal damage is ameliorated by quinacrine. Otamiri, T. Food Chem. Toxicol. (1989) [Pubmed]
  12. Effect of potassium deficiency and gossypol on urinary N-acetyl-beta-glucosaminidase excretion in the rat. Wu, D., Reidenberg, M.M. Contraception. (1993) [Pubmed]
  13. Possible biphasic changes of free radicals in ethylene glycol-induced nephrolithiasis in rats. Huang, H.S., Chen, C.F., Chien, C.T., Chen, J. BJU international. (2000) [Pubmed]
  14. An experimental model for studying reversible intestinal ischemia. Otamiri, T., Sjödahl, R., Tagesson, C. Acta chirurgica Scandinavica. (1987) [Pubmed]
  15. Different contributions of endothelin-A and endothelin-B receptors in the pathogenesis of deoxycorticosterone acetate-salt-induced hypertension in rats. Matsumura, Y., Hashimoto, N., Taira, S., Kuro, T., Kitano, R., Ohkita, M., Opgenorth, T.J., Takaoka, M. Hypertension (1999) [Pubmed]
  16. Hormonal regulation of isoenzymes of N-acetyl-beta-glucosaminidase and beta-galactosidase during spermatogenesis in the rat. Majumder, G.C., Lessin, S., Turkington, R.W. Endocrinology (1975) [Pubmed]
  17. Effects of OPC-21268, a vasopressin V1-receptor antagonist, on expression of growth factors from glomeruli in spontaneously hypertensive rats. Otsuka, F., Ogura, T., Yamauchi, T., Oishi, T., Hashimoto, M., Mimura, Y., Makino, H. Regul. Pept. (1997) [Pubmed]
  18. A novel N-acetylglucosaminidase from neonatal rat enterocytes. Jakoi, E.R., Brown, A.L. Biochem. Cell Biol. (1988) [Pubmed]
  19. Ultrastructural analysis of glycosaminoglycan hydrolysis in the rat periodontal ligament. I. Evidence for macrophage involvement in bone remodelling. Dorey, C.K., Bick, K.L. Calcified tissue research. (1977) [Pubmed]
  20. Lysophosphatidylcholine increases rat ileal permeability to macromolecules. Tagesson, C., Franzén, L., Dahl, G., Weström, B. Gut (1985) [Pubmed]
  21. Contrasting effects of gentamicin and mercuric chloride on urinary excretion of enzymes and phospholipids in the rat. Josepovitz, C., Levine, R., Lane, B., Kaloyanides, G.J. Lab. Invest. (1985) [Pubmed]
  22. Phospholipase A2 inhibition prevents mucosal damage associated with small intestinal ischaemia in rats. Otamiri, T., Lindahl, M., Tagesson, C. Gut (1988) [Pubmed]
  23. Deoxycholate depresses small-intestinal enzyme activity. Gracey, M., Houghton, M., Thomas, J. Gut (1975) [Pubmed]
  24. Dissociation of bile flow and biliary lipid secretion from biliary lysosomal enzyme output in experimental cholestasis. Lopez del Pino, V.H., LaRusso, N.F. J. Lipid Res. (1981) [Pubmed]
  25. Dual regulation by cAMP of beta-hexosaminidase-induced mitogenesis in bovine tracheal myocytes. Lew, D.B., Nebigil, C., Malik, K.U. Am. J. Respir. Cell Mol. Biol. (1992) [Pubmed]
  26. Hexosaminidase-altered aberrant crypts, carrying decreased hexosaminidase alpha and beta subunit mRNAs, in colon of 1,2-dimethylhydrazine-treated rats. Tsukamoto, T., Fukami, H., Yamanaka, S., Yamaguchi, A., Nakanishi, H., Sakai, H., Aoki, I., Tatematsu, M. Jpn. J. Cancer Res. (2001) [Pubmed]
  27. Regular structures in unit membranes. II. Morphological and biochemical characterization of two water-soluble membrane proteins isolated from the suckling rat ileum. Jakoi, E.R., Zampighi, G., Robertson, J.D. J. Cell Biol. (1976) [Pubmed]
  28. The relationship between lamellar bodies and lysosomes in type II pneumocytes. Gibson, K.F., Widnell, C.C. Am. J. Respir. Cell Mol. Biol. (1991) [Pubmed]
  29. Human serum contains a chitinase: identification of an enzyme, formerly described as 4-methylumbelliferyl-tetra-N-acetylchitotetraoside hydrolase (MU-TACT hydrolase). Overdijk, B., Van Steijn, G.J. Glycobiology (1994) [Pubmed]
  30. A postcoupling method for the demonstration of N-acetyl-beta-D-glucosaminidase in unfixed frozen tissue sections. Shannon, A.D. J. Histochem. Cytochem. (1975) [Pubmed]
 
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