Simonelli F, Cotticelli L, Pensa M, Teramo P, Acampora A, Rinaldi E
Boll Soc Ital Biol Sper. 1989 Aug;65(8):759-65.
To investigate the role of lipid peroxidation in diabetic cataractogenesis, malondialdehyde, a breakdown product of lipid peroxidation, was measured in lenses with incipient opacities and in retinas from diabetic rats and in clear lenses and in retinas from normal rats. The malondialdehyde mean values obtained in the transparent and cataractous lenses showed non-significant differences, while non-diabetic rat retinas had a significantly lower mean level of malondialdehyde compared with diabetic rat retinas (p less than 0.01). This indicates that, in streptozotocin-induced diabetic rats, lipid peroxidation is apparently not involved in the development of cataract, but it is quite probably involved in retinal damage. The retina, richer in polyunsaturated fatty acids than other ocular structures, is the elective site of lipid peroxidation and from this membrane peroxidation products might probably diffuse and damage other ocular tissues.
为研究脂质过氧化在糖尿病性白内障形成中的作用，对患有初期混浊的晶状体以及糖尿病大鼠视网膜中的脂质过氧化分解产物丙二醛进行了测定，并与正常大鼠的透明晶状体及视网膜进行比较。透明晶状体和白内障晶状体中的丙二醛平均值无显著差异，而与糖尿病大鼠视网膜相比，非糖尿病大鼠视网膜中的丙二醛平均水平显著较低（p<0.01）。这表明，在链脲佐菌素诱导的糖尿病大鼠中，脂质过氧化显然与白内障的发生无关，但很可能与视网膜损伤有关。视网膜比其他眼组织富含多不饱和脂肪酸，是脂质过氧化的选择性部位，膜过氧化产物可能从这里扩散并损害其他眼组织。
