Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighteen normal human eye-bank eyes (age: 18-81 years), five fetal eyes (16-24 weeks), 11 primary open-angle glaucoma (POAG) eyes (age: 76-89 years), and two Schnabel's cavernous optic atrophy eyes were examined using a biotinylated-hyaluronan binding protein to study the changes in the distribution of hyaluronic acid (HA) in the fetal, adult and glaucomatous optic nerve head. The vitreous body served as a positive control. Sections treated with Streptomyces hyaluronidase were used to confirm specificity. Monoclonal antibodies to myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) were used as additional controls. In fetal optic nerve, HA was localized in blood vessels, peripapillary sclera and the pial septae in the retrolaminar nerve. No staining was associated with axons. Staining for MBP was negative. In adults, HA was found surrounding the myelin sheaths in the retrolaminar nerve; staining decreased with age. In contrast, HA staining in myelinated peripheral nerves (e.g. ciliaries) remained unchanged with age. HA also was localized to the adventitia of arteries and veins throughout the posterior segment. Compared to age-matched normal eyes, HA staining was virtually absent around myelin sheaths of the retrolaminar nerve in POAG eyes. Similar changes were not found in other HA positive structures. In Schnabel's cavernous optic atrophy. HA was present in increased amount in the atrophic area, but virtually absent in the remaining retrolaminar nerve. HA staining was invariably positive in vitreous, and Streptomyces hyaluronidase treated sections were negative. In adults, staining of MBP was associated with the myelin sheath in the retrolaminar nerve. In contrast to HA, staining of MBP was unchanged with age and in POAG. In Schnabel's atrophy, MBP staining disappeared only in the atrophic area. HA in the retrolaminar optic nerve appears to be associate with the space-filling matrix between myelin sheaths. HA is not present in the axon bundles prior to myelination of the optic nerve. HA in the retrolaminar optic nerve appears to decrease with age and is further reduced in POAG; however, corresponding changes are not found in MBP or in peripheral nerves. Perhaps, decreased amounts of HA is related to a higher susceptibility to elevated intraocular pressure or to optic nerve atrophy. In Schnabel's cavernous optic atrophy, HA is present in increased amount only in the atrophic area while MBP is markedly decreased, suggesting in situ production of HA in areas of optic nerve atrophy.
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PMID:Hyaluronic acid in the normal and glaucomatous optic nerve. 922 77

We determined the effect of chronic and acute loss of glycosaminoglycans from the aqueous outflow pathway on intraocular pressure (IOP) and outflow facility in the subhuman primate eye. For the study of the chronic effects of the GAGases, cynomolgus monkeys received intracameral injections of hyaluronidase (Streptomyces, 5 or 50 units, n=2) or chondroitinase ABC (0.05 or 0.25 units, n=2) biweekly for 8 months (4 months for each dose). IOP was measured at 3, 7, 10 and 14 days after each injection. Outflow facility (2-level constant pressure) was determined at 2, 4, 6, and 8 months. Monkeys were killed 6 days after the last injection. The changes in the distribution of hyaluronic acid and sulfated proteoglycans in the outflow pathway were examined using substrate-specific histochemical techniques. The acute effects of these enzymes on outflow facilities (30 min or 2 hr after enzyme) were determined in another group of animals (n=4 for each time enzyme-1). IOP and outflow facility were unchanged compared to controls (heat inactivated enzyme) at any time in the chronically or acutely treated monkeys. Hyaluronic acid staining was absent in the outflow pathways of eyes treated chronically with hyaluronidase compared with control eyes, while collagen-associated sulfated proteoglycans were decreased but not completely removed by the chronic chondroitinase ABC treatment. Chronic loss of these glycosaminoglycans from the trabecular meshwork does not appear to contribute to the IOP elevation and decrease in outflow facility that accompanies open-angle glaucoma. Most importantly, no increase in outflow facility was found with acute hyaluronidase or chondroitinase treatment.
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PMID:Intraocular pressure and outflow facility are unchanged following acute and chronic intracameral chondroitinase ABC and hyaluronidase in monkeys. 926 86

We evaluated the effects of three specific glycosaminoglycan-degrading enzymes, chondroitinase ABC, testicular hyaluronidase, and heparinase, on the intraocular pressure (IOP) and the anterior chamber structures of bovine eyes. The anterior segment of freshly enucleated bovine eyes was perfused in a modified organ culture system. After each enzyme solution or its corresponding vehicle was introduced into the anterior chamber, the IOP was monitored for </=6 h. Compared to the control group, the chondroitinase ABC-treated group showed a significant IOP reduction after 1 h of perfusion. Testicular hyaluronidase and heparinase did not show any significant effect. Light microscopy revealed that chondroitinase ABC and testicular hyaluronidase induced detachment of the endothelial cells from trabecular beams in the uveal meshwork. Disruption of the tissues in the juxtacanalicular region and fragmentation of the endothelial cells facing the angular aqueous plexus were observed in the chondroitinase ABC- and heparinase-treated specimens. Electron microscopic study revealed detachment of trabecular meshwork cells from the beams and rupture of the inner wall of the aqueous plexus in all the enzyme-treated eyes. Cellular organelles and architectures were better preserved in chondroitinase ABC-treated eyes than those treated with hyaluronidase and heparinase. These results indicate that chondroitinase ABC has a pronounced effect on the IOP with relatively minor effect on the trabecular meshwork structures.
J Glaucoma 1993
PMID:Effects of glycosaminoglycan-degrading enzymes on bovine trabecular meshwork in organ culture. 1992 Apr 91

Hyaluronidase is a bovine or ovine testicular protein that is used as an adjunct to co-administered medicaments and fluids to enhance their dispersion and absorption through the degradation of hyaluronan. While it is a known potential allergen, there are few reports of hyaluronidase hypersensitivity. A 56-year-old lady presented 8 hours post glaucoma surgery with ipsilateral lacriminorrhoea, periorbital erythema, oedema, proptosis, pruritus and conjunctival chemosis. Right ocular motility was restricted and visual acuity was reduced. The reaction settled with oral corticosteroids and antihistamines. Hyaluronidase allergy was confirmed on skin prick testing. Hyaluronidase allergy is rare. In the few cases reported, reactions occurred at various doses and were acute (intraoperative), early (within hours), intermediate (within days) or delayed (within weeks). Anaphylaxis has also been described. Primary sensitization appears to be a prerequisite for most reactions. The variability in onset of symptoms and the response to skin testing would suggest that type I and type IV hypersensitivity may both contribute to this response. In this case, the timing fitted with a late phase type 1 reaction. This case shows that despite being less common than haemorrhage for acute reactions and infection for delayed reactions, allergy can account for orbital inflammation following ophthalmic surgery.
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PMID:Hyaluronidase allergy: a rare cause of periorbital inflammation. 2014 44


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