*A preliminary version of this paper was presented at the International Symposium on Retinal Degeneration, San Francisco, CA, 1988. The proceedings are to be published by Alan R. Liss, New York.
HEMOPROTEIN(S) MEDIATE BLUE LIGHT DAMAGE IN THE RETINAL PIGMENT EPITHELIUM*
Article first published online: 2 JAN 2008
Photochemistry and Photobiology
Volume 51, Issue 5, pages 599–605, May 1990
How to Cite
Pautler, E. L., Morita, M. and Beezley, D. (1990), HEMOPROTEIN(S) MEDIATE BLUE LIGHT DAMAGE IN THE RETINAL PIGMENT EPITHELIUM. Photochemistry and Photobiology, 51: 599–605. doi: 10.1111/j.1751-1097.1990.tb01972.x
- Issue published online: 2 JAN 2008
- Article first published online: 2 JAN 2008
- Received 8 September 1989; accepted 8 December 1989
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. A decrease in leucine transport was also noted, but the effect required10–30 min of exposure to be manifested on some occasions. Utilizing the observed depolarizing effect of blue light, an action spectrum was determined which encompasses the absorption spectrum of the oxidized and reduced forms of cytochrome c oxidase. O2 uptake studies on isolated pigment epithelial cells verified the reduction of respiration by exposure to blue light, which is observed in other cells. Ultrastructural studies revealed that the major cytopathology observed up to 60 min after blue light exposure was a blistering of the mitochondria which progressed to a swollen, disrupted state within the post irradiation period of 1 h. Comparison of these results with those of other studies suggests that the mechanism of UV-A damage differs substantially from that of blue light.