| First Author | Bai S | Year | 2013 |
| Journal | Exp Eye Res | Volume | 108 |
| Pages | 76-83 | PubMed ID | 23274583 |
| Mgi Jnum | J:210431 | Mgi Id | MGI:5571035 |
| Doi | 10.1016/j.exer.2012.12.007 | Citation | Bai S, et al. (2013) NAD(+) maintenance attenuates light induced photoreceptor degeneration. Exp Eye Res 108:76-83 |
| abstractText | Light-induced retinal damage (LD) occurs after surgery or sun exposure. We previously showed that zinc (Zn(2+)) accumulated in photoreceptors and RPE cells after LD but prior to cell death, and pyruvate or nicotinamide attenuated the resultant death perhaps by restoring nicotinamide adenine dinucleotide (NAD(+)) levels. We first examined the levels of NAD(+) and the efficacy of pyruvate or nicotinamide in oxidative toxicities using primary retinal cultures. We next manipulated NAD(+) levels in vivo and tested the affect on LD to photoreceptors and RPE. NAD(+) levels cycle with a 24-h rhythm in mammals, which is affected by the feeding schedule. Therefore, we tested the affect of increasing NAD(+) levels on LD by giving nicotinamide, inverting the feeding schedule, or using transgenic mice which overexpress cytoplasmic nicotinamide mononucleotide adenyl-transferase-1 (cytNMNAT1), an NAD(+) synthetic enzyme. Zn(2+) accumulation was also assessed in culture and in retinal sections. Retinas of light damaged animals were examined by OCT and plastic sectioning, and retinal NAD(+) levels were measured. Day fed, or nicotinamide treated rats showed less NAD(+) loss, and LD compared to night fed rats or untreated rats without changing the Zn(2+) staining pattern. CytNMNAT1 showed less Zn(2+) staining, NAD(+) loss, and cell death after LD. In conclusion, intense light, Zn(2+) and oxidative toxicities caused an increase in Zn(2+), NAD(+) loss, and cell death which were attenuated by NAD(+) restoration. Therefore, NAD(+) levels play a protective role in LD-induced death of photoreceptors and RPE cells. |
