Investigation of Laser-Induced Retinal Damage
Abstract
Laser-induced damage in ocular tissue was studied with biochemical measures designed to characterize cellular damage mechanisms. Photochemical damage was identified by evidence of oxidative reactions resulting from photosensitizers and free radicals activated by the light exposure. Melanin, in the retinal pigment epithelial (RPE) cells, during illumination formed a free radical that rapidly oxidized ascorbic acid (AA). This specific reaction may safely direct excess photons into a chain of coupled redox reactions. RPE cells have a high capacity for utilizing AA; the cells have different transporters for AA and its oxidized form, dehydro-L-ascorbic acid (DHA), and are able to reduce DHA to AA. The kinetics of these transporters were measured in these studies. Light-activated melanin was also shown to react with linoleic acid, a model lipid. Thus, in the absence of sufficient AA, the melanin radical may initiate lipid peroxidation, a known concomitant of photochemical damage. Development of assays indicative of thermal damage was also started Initial results suggested that extracellular potassium ion concentration increased following laser-induced thermal stress in RPE cells. This change was hypothesized to result from damage to sodium-potassium ionic pumps in the cell's plasma membrane.... Laser bioeffects, Photochemical, Thermal, Photooxidation, Melanin, Ascorbic acid, Linoleic acid.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 20, 1993
- Accession Number
- ADA264096
Entities
People
- Kwok-wai Lam
- Randolph D. Glickman
Organizations
- University of Texas Health Science Center at San Antonio