Shvedova A A, Alekseeva O M, Muranov K O, Kagan V E
Curr Eye Res. 1982;2(10):683-9. doi: 10.3109/02713688209019997.
It has been shown that illumination of rod outer segment suspension in the presence of photosensitizers (methylene blue lambda greater than or equal to 620 nm; retinal 370 less than or equal to lambda less than or equal to 390 nm) results in chemical modification of the lipid and protein components of the photo-receptor membranes. This modification can be registered by accumulation of lipid peroxidation (LPO) products as well as oligomerization of rhodopsin and a decrease of rhodopsin thermal stability. These effects are prevented by 'O2-quenchers and free radical scavengers. It has been found that the electric activity (ERG) of isolated frog retina is inhibited due to photosensitized generation of 'O2 which can be overcome by preliminary addition of 'O2-quenchers and free radical scavengers to the incubation medium. The LPO products are accumulated in the retinae of rats exposed to high intensity light in vivo. It is concluded that 'O2 and LPO are involved in light-induced damage of the retina.
研究表明，在存在光敏剂（亚甲蓝，λ≥620nm；视黄醛，370≤λ≤390nm）的情况下，对杆状外段悬浮液进行光照会导致光感受器膜的脂质和蛋白质成分发生化学修饰。这种修饰可通过脂质过氧化（LPO）产物的积累、视紫红质的寡聚化以及视紫红质热稳定性的降低来记录。这些效应可被“O2猝灭剂”和自由基清除剂所阻止。研究发现，由于光敏化产生“O2”，离体青蛙视网膜的电活动（ERG）受到抑制，而在孵育介质中预先添加“O2猝灭剂”和自由基清除剂可克服这一现象。LPO产物在体内暴露于高强度光的大鼠视网膜中积累。得出的结论是，“O2”和LPO参与了光诱导的视网膜损伤。
