Accession Number:

ADA285186

Title:

Investigation of Laser-Induced Retinal Damage: Wavelength and Pulsewidth Dependent Mechanisms

Descriptive Note:

Final technical rept. 1 Apr 1991-31 Mar 1994

Corporate Author:

TEXAS UNIV HEALTH SCIENCE CENTER AT SAN ANTONIO

Personal Author(s):

Report Date:

1994-08-31

Pagination or Media Count:

20.0

Abstract:

This research was initiated to develop biochemical and cellular assays of laser damage in ocular tissue. Photochemical damage was identified by evidence of oxidative reactions resulting from free radicals generated by the interaction of laser and incoherent light with ocular tissue components. Melanin contained in retinal pigment epithelial RPE cells formed a free radical during illumination and rapidly oxidized ascorbic acid AA. 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 efficiently reduce DHA to AA. The kinetics and specificity of these transporters were measured in these studies. In the absence of AA or other antioxidants, light-activated melanin promoted the formation of hydroperoxides of the fatty acid, linoleic acid. Thus, if intracellular antioxidants become depleted, the melanin radical may mediate some aspects of photochemical damage such as lipid peroxidation. Other assays of laser damage were investigated. Following laser exposure, release of K ions from RPE cells could be demonstrated, but the measured changes were small and inconsistent. Efflux of the cytoplasmic enzyme, lactate dehydrogenase, showed more promise as an assay for thermal or photodisruptive laser bioeffects. Laser bioeffects, Photochemical, Thermal, Melanin, Free radical, Ascorbic acid, Linoleic acid, Photosensitizer.

Subject Categories:

  • Stress Physiology
  • Lasers and Masers

Distribution Statement:

APPROVED FOR PUBLIC RELEASE