STRESS-WAVE-INDUCED INJURY TO RETINAL-PIGMENT EPITHELIUM-CELLS IN-VITRO

Citation
T. Douki et al., STRESS-WAVE-INDUCED INJURY TO RETINAL-PIGMENT EPITHELIUM-CELLS IN-VITRO, Lasers in surgery and medicine, 19(3), 1996, pp. 249-259
Citations number
33
Categorie Soggetti
Medical Laboratory Technology",Surgery
ISSN journal
01968092
Volume
19
Issue
3
Year of publication
1996
Pages
249 - 259
Database
ISI
SICI code
0196-8092(1996)19:3<249:SITREI>2.0.ZU;2-#
Abstract
Background and Objective: To determine the survival of in vitro retina l pigment epithelium (RPE) cells subjected to laser-generated stress t ransients (shock waves) and compare it to that of other cell lines. St udy Design/Materials and Methods: Normal and transformed human retinal pigment epithelium cell lines were used. The cells were imbedded in a gel to prevent motion and cavitation and located in a thin layer at t he bottom of a pipette tube closed at one end by a polyimide film. Str ess transients were generated by pulsed excimer laser (193 nn and 248 nm wavelength) ablation of the polyimide film. Cell survival, compared to that of unirradiated cells, was assessed by counting surviving cel ls. The stress was varied from 300 to 740 bars and the number of shock wave pulses applied varied from 5 to 150. Results: Cell survival decr eased sharply at the higher stresses but some cells always survived. T he lowest survival rate was 50%. Increasing the number of shock wave p ulses did not increase cell killing after 20 pulses, demonstrating a s aturation effect. In contrast to the transformed cell Line, normal cel ls could not be killed at the highest stress available to us. Conclusi on: The susceptibility of RPE cells to damage by stress waves varies w ith cell. line. Transformed retinal pigment epithelium cells are more susceptible than normal ones. Saturation of the damage versus number o f pulses is observed and a threshold-like behavior for cell killing ve rsus stress is found. Because at least 50% of the cells survived, norm al cell growth can serve to replenish damaged cells. (C) 1996 Wiley-Li ss, Inc.