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

Facility of aqueous outflow and time-dependent changes in its hyaluronidase-sensitive and hyaluronidase-resistant components were evaluated in freshly excised canine eyes by constant pressure quantitative aqueous perfusion. Mean baseline facility of outflow was 0.24 microliter/min/mm Hg. With prolonged perfusion at constant intraocular pressure, facility of outflow was observed to increase almost linearly for at least 3 hr and continued to increase for up to 10 hr, reaching a maximum several times the initially measured facility. Perfusion with pooled dog aqueous humor did not prevent the time-dependent increase in measured facility. Rapid exchange of anterior chamber contents with perfusion solution alone produced an immediate threefold increase in facility, again followed by a gradual time-dependent facility increase. Rapid exchange of anterior chamber contents with hyaluronidase produced an immediate fivefold increase in facility with stabilization of measured facility over 3 hr and subsequent perfusion. The time-dependent changes in measured facility of outflow or "washout phenomenon" appeared to result from the gradual dissolution of the hyaluronidase-sensitive component of the barriers to aqueous outflow in the canine eye.
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PMID:The canine eye: in vitro dissolution of the barriers to aqueous outflow. 14 84

Several sulfhydryl reactive compounds have previously been shown to influence aqueous humor outflow facility. The purpose of the current study was to investigate the effect of glutathione depletion on certain of these sulfhydryl actions. Enucleated calf, monkey, and human eyes were perfused via the anterior chamber by the constant pressure (15 mmHg) technique. In calf eyes, perfusion of 10 mM cysteamine produced a small (-23%, P = 0.03) decrease in outflow facility that was also observed after hyaluronidase pretreatment. In contrast, following pretreatment with 1 mM BCNU [1,3 bis(2 chlorethyl)-1-nitrosourea], an inhibitor of glutathione reductase, and 10 mM diamide, a glutathione oxidant, which did not by themselves significantly affect outflow facility, perfusion of cysteamine resulted in an opposite effect--a remarkably large (+90%, P less than 0.001) increase in outflow facility. Other reduced and oxidized sulfhydryl-containing compounds such as cysteine, beta-mercaptoethanol, and glutathione, itself, as well as the non-sulfhydryl reducing agent, ascorbic acid, were substituted for cysteamine in this protocol and found to produce similar effects of varying magnitudes. In general, the reduced sulfhydryl containing compounds and ascorbic acid were the most effective. Pretreatment with BCNU alone without diamide did not produce this effect. Treatment with BCNU and diamide resulted in a greater than 75% decrease in reduced glutathione levels and a concomitant tenfold increase in glutathione mixed disulfide levels (0.229 vs. 0.030 mumol g-1 wet weight) in the calf trabecular meshwork. The subsequent perfusion with cysteamine reversed this mixed disulfide formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influences of glutathione and sulfhydryl containing compounds on aqueous humor outflow function. 216 47

The behavior of sodium hyaluronate injected into the anterior chamber of rabbits was investigated using a 1% (w/v) solution of sodium hyaluronate having a molecular weight of 800K. Although the aqueous humor contained a considerable amount of reduced ascorbic acid, the molecular weight of sodium hyaluronate injected into the anterior chamber did not change. This was due to existence of a protecting factor for degradation of sodium hyaluronate in a low molecular weight fraction of the aqueous humor. The injected sodium hyaluronate was found to aggregate with proteins in the aqueous humor within 2 hrs. However, this aggregation did not affect the degradation of sodium hyaluronate with ascorbic acid. The hyaluronic acid content in the iris-ciliary body increased about three times as much as the normal level 2 hrs after the sodium hyaluronate injection. This result suggests that the injected sodium hyaluronate is not only eliminated through the angular aqueous plexus but also through the iris-ciliary body, followed by digestion with hyaluronidase in those tissues.
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PMID:Biochemical studies on the use of sodium hyaluronate in the anterior eye segment. II. The molecular behavior of sodium hyaluronate injected into anterior chamber of rabbits. 671 59