N-acetylcysteine amide (NACA) Prevents Retinal Degeneration Induced by Sodium Iodate in C57BL/6 Mice

Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly. AMD is a degenerative condition that begins in %UXFK¶V PHPEUDQH and progresses to the retinal pigment epithelium (RPE) and, ultimately, the overlying photoreceptors. Since oxidative stress is strongly implicated in the pathogenesis of AMD, we hypothesized that N-acetylcysteine amide (NACA), a novel thiol antioxidant, would retard progression of retinal degeneration. in order to assess whether NACA had a significant impact on prevention of sodium iodate (NaIO3)-induced (50mg/kg) retinal degeneration, we utilized 2-month-old C57BL/6 mice which were divided into a control group, a NACA-only group, a NaIO3-induced retinal degeneration group, and a NACA-treated retinal degeneration group. We measured the degrees of photoreceptor cell death and function in the mice using both an electroretinogram (ERG) and analysis of photoreceptor histology, the thickness of the outer nuclear layer (ONL). Our results indicated that treatment with NACA eye drops significantly prevented the reduction in mean peak amplitude of scotopic and photopic waves and reduction in ONL thickness induced by sodium iodate. NACA demonstrated preservation of visual potential and the photoreceptor function in the NaIO3-induced retinal degeneration. in addition, NACA was able to increase the retinal glutathione (GSH) levels in NaIO3treated mice. These results illustrated that NACA can prevent photoreceptor degeneration and loss of visual potential in vivo and, therefore, this nontoxic and potent antioxidant should be considered for the treatment of AMD