PHOTIC INJURY TRIGGERS APOPTOSIS OF PHOTORECEPTOR CELLS

Apoptosis, a highly regulated and energy-dependent process of cell dea th, plays an important part in normal tissue development. Its role in pathological conditions may vary. Earlier morphologic studies suggest that apoptosis may be an important mechanism in light-induced photorec eptor degeneration. In this study, we determined if photic exposure tr iggers apoptosis in photoreceptor cells in an established model of pho toteceptor degeneration by light exposure. Twenty eight Lewis albino r ats were divided into seven groups of 4 animals each: one group served as the unexposed control; and the other groups were exposed continuou sly to green fluorescent light (320 foot-candles) for 3, 6, 9, 12, 18 or 24 hours, respectively and killed for histopathological examination , biochemical isolation of retinal DNA; and in situ analysis of nicked nuclear DNA by terminal transferase biotin-dUTP nick end labeling (TU NEL). Histopathological study revealed morphological changes comparabl e to previous reports on photic injury. Electrophoretic analysis of DN A showed internucleosomal DNA cleavage as early as 12 hours of light e xposure. The fluorescent intensity of DNA fragments, which were monome rs and multimers of 180-200 base pairs, increased with the duration of light exposure. TUNEL technique, which localized DNA cleavage to the photoreceptor cell nuclei as early as 6 hours of light exposure, showe d that the number of TUNEL positive nuclei increased with light exposu re, and revealed more DNA degradation in the superior quadrant. Our fi ndings confirmed earlier morphologic observations that photic exposure triggers apoptosis of photoreceptor cells.