Photic injury triggers apoptosis of photoreceptor cells

Apoptosis, a highly regulated and energy-dependent process of cell death, 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 photoreceptor degeneration. In this study, we determined if photic exposure triggers apoptosis in photoreceptor cells in an established model of photoreceptor degeneration by light exposure. Twenty eight Lewis albino rats were divided into seven groups of 4 animals each: one group served as the unexposed control; and the other groups were exposed continuously 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 (TUNEL). Histopathological study revealed morphological changes comparable to previous reports on photic injury. Electrophoretic analysis of DNA showed internucleosomal DNA cleavage as early as 12 hours of light exposure. The fluorescent intensity of DNA fragments, which were monomers 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, showed that the number of TUNEL positive nuclei increased with light exposure, and revealed more DNA degradation in the superior quadrant. Our findings confirmed earlier morphologic observations that photic exposure triggers apoptosis of photoreceptor cells.