Abstract
Purpose: :
To investigate mechanism of photoreceptor degeneration, this study was experimented using the sodium iodate treated retina in rat.
Methods: :
Male SD rats (8weeks old) were intraperitoneally injected 50mg/kg. The retina was collected for microscopy and gene expression at 24hrs after sodium iodate treatment. For microscopy, the retinas were fixed and observed by light microscope and electron microscope. For gene expression, total RNA and protein were extracted from retina and RT–PCR and immunobloting were performed.
Results: :
Retinal degeneration was observed by light microscope in sodium iodate treated rat. Retinal pigment epithelial cells and photoreceptors were damaged. Several genes were decreased in sodium iodate treated retina. However, guanylyl cyclase, cGK1 and arrestin were increased. The guanylyl cyclase was increased in dose dependent manner. And the methylene blue was intraperitoneally treated for inhibition of guanylyl cyclase. The methylene blue protected sodium iodate induced retinal degeneration.
Conclusions: :
In this study, inhibition of guanylyl cyclase protects retinal degeneration in sodium iodate toxicity. Therefore, these results suggest that the guanylyl cyclase is a key mediator in sodium iodate toxicity or photoreceptor degeneration.
Keywords: photoreceptors • degenerations/dystrophies • retinal degenerations: cell biology