Purpose. We recently found that continuous light exposure at a moderat
e intensity triggered apoptosis of photoreceptor cells. Since intermit
tent light exposure is known to cause more severe retinal damage than
is continuous light exposure, we sought to determine if intermittent l
ight exposure also triggered apoptosis of photoreceptor cells. Methods
. Lewis albino rats were reared, for 2 weeks, in cyclic light and dark
adapted for 24 hr before light exposure. Rats were exposed to intermi
ttent light or continuous light for 6 or 9 hr, respectively. Light-exp
osed rats were killed by lethal injection at three timepoints: immedia
tely after light exposure, after 6 hr of dark recovery following light
exposure and after 24 hr of dark recovery following light exposure. R
etinal damage after light exposure was evaluated by morphology, morpho
metry, the terminal transferase-mediated biotin dUTP nick end labeling
(TUNEL) technique for identification of nicked/cleaved nuclear DNA an
d agarose gel electrophoresis of retinal DNA. Results. Evaluation of m
orphology confirmed that intermittent light exposure caused more photo
receptor cell damage than did continuous light exposure of the same du
ration and intensity. The TUNEL technique showed that photoreceptor nu
clei contained nicked or cleaved DNA after either intermittent or cont
inuous light exposure, although more TUNEL-positive nuclei were observ
ed after intermittent exposure. Agarose gel electrophoresis of retinal
DNA showed internucleosomal DNA fragmentation, which is associated wi
th apoptosis in samples from intermittent light exposure. Conclusions.
These data demonstrated that intermittent light exposure triggered ap
optosis in more photoreceptor cells than did continuous light exposure
of the same intensity and duration.