Change of redox status and modulation by thiol replenishment in retinal photooxidative damage.

摘要: PURPOSE. Cellular or tissue reduction-oxidation (redox) is crucial in various diseases. The present study was conducted to analyze how redox status affected by photooxidative stress and whether the exogenous thiol antioxidant N-acetylcysteine (NAC) affects stress-induced retinal damage. METHODS. Mice were intraperitoneally injected with either NAC (250 mg/kg) phosphate-buffered saline (PBS) exposed white fluorescent light (8000 lux) for 2 hours. Levels of thioredoxin (TRX), glutaredoxin (GRX), glutathione (GSH), endogenous regulators redox; 4-hydroxy-2-nonenal (HNE)-modified protein, a marker lipid peroxidation; nuclear factor (NF)-B, redox-sensitive transcription samples, measured immunohistochemistry Western blot enzymatic recycling assay. Light-induced damage estimated electroretinography quantitative 8-hydroxy-2-deoxyguanosine (8OHdG index), oxidative DNA damage, compared NAC- PBS-treated mice. RESULTS. Upregulation TRX HNE-modified decrease GSH, translocation NF-B noted after exposure These changes suppressed NAC-treated mice GRX not upregulated any a- b-wave amplitudes significantly higher, 8OHdG index lower than CONCLUSIONS. Retinal altered intense normalized partially effect on GSH levels. Manipulation state replenishment may be useful strategy prevent (Invest Ophthalmol Vis Sci. 2002;43:2392‐2400)