CARBONIC-ANHYDRASE ACTIVITY IS INCREASED IN RETINAL PIGMENTED EPITHELIUM AND CHORIOCAPILLARIS OF RCS RATS

Citation
M. Eichhorn et al., CARBONIC-ANHYDRASE ACTIVITY IS INCREASED IN RETINAL PIGMENTED EPITHELIUM AND CHORIOCAPILLARIS OF RCS RATS, Graefe's archive for clinical and experimental ophthalmology, 234(4), 1996, pp. 258-263
Citations number
23
Categorie Soggetti
Ophthalmology
ISSN journal
0721832X
Volume
234
Issue
4
Year of publication
1996
Pages
258 - 263
Database
ISI
SICI code
0721-832X(1996)234:4<258:CAIIIR>2.0.ZU;2-3
Abstract
Background: In Royal College of Surgeons (RCS) rats the retinal pigmen ted epithelium (RPE) exhibits defective phagocytosis of rod outer segm ents, causing degeneration of the photoreceptor layer. It is not known whether another function of the RPE, ion and fluid transport, is also affected by the disease. One enzyme involved in modulation of RPE tra nsport activities is carbonic anhydrase (CA). To clarify whether chang es in CA activity are correlated with the process of retinal degenerat ion, the localization of CA activity in RCS rat eyes was investigated. Methods: Eyes of 12 RCS rats and 12 age-matched congenic controls of different ages were studied, using a modified histochemical method of Hansson for light and electron microscopy. Results: Control eyes showe d CA staining in corneal endothelium, both layers of ciliary epitheliu m, Muller cells, inner segments of photoreceptors, and RPE cells. In R PE the apical membranes were most intensely stained. In RCS rats, chan ges in CA staining were seen only in the posterior segment of rats 6 a nd 7 months of age. Most of the RPE cells were more intensely stained than those of age-matched controls, especially due to increased CA act ivity in the basolateral membrane infoldings. Adjacent endothelial cel ls of the choriocapillaris and of retinal capillaries developed staini ng for CA activity. Conclusion: Changes in CA activity in the RPE and adjacent capillary endothelium, together with previously described cha nges in RPE morphology in RCS rats, indicate changes in ion and fluid transport across the RPE. Since the retina was already impaired when t he increase in CA activity occurred, we hypothesize that the causative factor is not the genetic defect per se, but the destruction of the r etina.