Akiba J, Yanagiya N, Kakehashi A, Hikichi T, Kado M, Yoshida A, Ueno N
Department of Ophthalmology, Asahikawa Medical College, Japan.
Ophthalmic Res. 1997;29(1):37-41. doi: 10.1159/000267989.
To investigate copper-ion (Cu2+)-catalyzed vitreous liquefaction in vivo, Cu2+ solution (10 mumol) was injected into the vitreous cavity of rabbits. At 24 h after the injection, the gel and liquid vitreous were weighed, and the percent of vitreous liquefaction was calculated. Cu2+ injection resulted in liquefaction of 58% of the vitreous, although control eyes had 12% liquefaction (p < 0.1). The vitreous liquefaction was more pronounced in the presence of exogenous ascorbic acid. However, the addition of mannitol, a hydroxyl-radical-specific scavenger, significantly suppressed the Cu(2+)-catalyzed vitreous liquefaction. The free radicals generated by the Cu(2+)-catalyzed oxidation system may cause vitreous liquefaction in vivo.
为了研究铜离子（Cu2+）在体内催化玻璃体液化的情况，将Cu2+溶液（10微摩尔）注入兔眼玻璃体腔。注射后24小时，称量凝胶状和液态玻璃体的重量，并计算玻璃体液化的百分比。注射Cu2+导致58%的玻璃体液化，而对照眼的液化率为12%（p<0.1）。在外源性抗坏血酸存在的情况下，玻璃体液化更为明显。然而，添加甘露醇（一种羟基自由基特异性清除剂）可显著抑制Cu(2+)催化的玻璃体液化。Cu(2+)催化氧化系统产生的自由基可能在体内导致玻璃体液化。
