Abstract
Abstract: :
Purpose: To determine the protective role of thioredoxin (TRX) against retinal light damage in mice. Methods: Four-week-old BALB/c mice were exposed to white fluorescent light (8,000 lux) for 2 hours. The number of both the photoreceptor cell nuclei and the TUNEL-positive photoreceptor cell nuclei were counted to determine the severity of damage. Expression of endogenous TRX was analyzed in the retinal samples by immunohistochemistry and Western blot. Recombinant TRX (rTRX) or mutant rTRX, in which cysteines in the active site are replaced with serines, was injected intravitreously into BALB/c mice before light exposure. Oxidized and tyrosine-phosphorylated proteins were analyzed in retinal samples to examine the antioxidative effect of TRX. The number of photoreceptor cell nuclei and the DNA ladder in the retinal samples were analyzed.Results: We observed a significant reduction in the number of photoreceptor cells and induction of TUNEL-positive nuclei after light exposure. TRX expression was enhanced in both the neural retina and retinal pigment epithelium after light exposure. The amounts of oxidized and tyrosine-phosphorylated proteins decreased in the neural retinas of the rTRX-treated mice compared to the vehicle- or mutant rTRX-treated mice. The reduction of photoreceptor cells and formation of a DNA ladder were suppressed by rTRX pretreatment but not with mutant rTRX.Conclusion: TRX is induced in the retinal tissue after light exposure. Intraocular injection of rTRX suppress photooxidative stress. TRX intensification may be a useful therapeutic strategy to prevent retinal light damage.
Keywords: 321 antioxidants • 323 apoptosis/cell death • 554 retina