The potentiating effects of ethanol on the blue light depolarization of the retinal pigment epithelium.

The retinal pigment epithelium (RPE) is the site of two major effects of ethanol. In humans, ethanol produces a slow damped oscillation in the steady electrical potential of the eye, which is generated primarily by the RPE. It has also been shown that ethanol potentiates the reversible, depolarizing effect of blue light on the transepithelial potential (TEP) of the isolated RPE.

The effects of retina-derived factors on the electrical and ultrastructural properties of the bovine pigment epithelium.

The transepithelial potential (TEP) and short circuit current (SCC) of the bovine retina pigment epithelium (RPE) were monitored throughout a 3hr period. Application of retina-derived factors to the apical side of the preparation resulted in a stabilization of the TEP and SCC, followed by a secondary rise in both electrical parameters. The late, secondary rise could be eliminated or reduced by the administration of cycloheximide suggesting a dependence upon protein synthesis.

Hemoprotein(s) mediate blue light damage in the retinal pigment epithelium.

In order to elucidate the mechanisms of blue light damage on ocular tissues, the transepithelial transport, electrical characteristics and ultrastructural properties of irradiated isolated bovine retinal pigment epithelium (RPE) were investigated. Blue light (430 nm) irradiation at 20 mW/cm2 significantly reduced the transepithelial potential and short circuit current of RPE. During blue light exposure, a decrease in chloride transport was observed, and this decrease appeared to be closely coupled to changes in the electrical properties of the pigment epithelium.

Modification of leucine transport across bovine pigment epithelium by metabolic stress.

The transport of leucine in the apical-to-basal (retina to choroid) direction across the isolated bovine retinal pigment epithelium is mediated predominantly by the L amino transport system at low carrier (10 microns) concentrations. There is no evidence of an active or facilitated transport system operating in the opposite direction. The identification of the L system is based on the lack of sodium dependence, specific inhibition of leucine transport by 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH), and the demonstration of trans-stimulation.