Defects in cortisol-metabolizing enzymes in primary open-angle glaucoma.
Assays of cortisol-metabolizing enzymes in homogenates of human trabecular meshwork cells under optimal conditions revealed two defects in primary open-angle glaucoma (POAG): one is a marked increase in delta 4-reductase and the other is a decrease in 3-oxidoreductase. Experiments indicated that the differences in enzyme activities seen between POAG and nonPOAG trabecular meshwork derived cell homogenates were due to altered amounts of enzymes rather than to alterations in cofactor availability, pH, or endogenous activators or inhibitors. This clearly demonstrates an enzymatic defect(s) in POAG which may be the basis for the ocular hypertension and sensitivity to exogenous glucocorticoids seen in this disorder.
D005902:Glaucoma, Open-Angle / Q000201:enzymology*; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D009798:Ocular Hypertension / Q000209:etiology / Q000378:metabolism; D010088:Oxidoreductases / Q000378:metabolism*; D011965:Receptors, Glucocorticoid / Q000187:drug effects; D014129:Trabecular Meshwork / Q000201:enzymology*
D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D010088:Oxidoreductases; C034519:cortisol delta 4-reductase