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以胆固醇为对照，研究动脉粥样硬化症中常见的两种氧化型胆固醇（３β，５α，６β－三羟胆固烷、２５－羟胆固醇）对血管平滑肌细胞损伤及损伤机制。结果表明，于损伤早期，细胞的谷胱甘肽过氧化物酶活性增高，还原型谷胱甘肽含量减少。损伤后期谷胱甘肽过氧化物酶活性下降，细胞谷胱甘肽耗竭，细胞总巯基含量下降，细胞脂质过氧化产物含量和细胞羰基含量明显增高，表明细胞出现严重的氧化性损伤。而纯胆固醇，在与这两种氧化型胆固醇相同的作用时间，作用条件及剂量大于这两种氧化型胆固醇两倍以上的情况下，未曾引起细胞抗氧化酶、谷胱甘肽、蛋白质及脂质的任何明显改变。外给金属硫蛋白可减轻细胞损伤，外给Ｌ－ｂｕｔｈｉｏｎｅｉｎ－［Ｓ，Ｒ］－ｓｕｌｆｏｘｉｍｉｎｅ使细胞损伤加重，说明损伤与巯基含量有关。结果提示氧化型胆固醇引起的细胞损伤可能是通过氧应激产生。
Cholesterol as a control, atherosclerosis in common two kinds of oxidized cholesterol (3β, 5α, 6β-tricine, 25-hydroxycholesterol) on vascular smooth muscle cell injury and injury mechanism. The results showed that in the early injury, the cells increased glutathione peroxidase activity, reduced glutathione content. Glutathione peroxidase activity decreased, glutathione depletion, total sulfhydryl content decreased, lipid peroxidation product content and cell carbonyl content increased significantly in the late stage of injury, indicating that the cells had serious oxidative damage. Cholesterol, however, did not cause cellular anti-oxidase, glutathione, protein and lipid in the same duration of action, action and dosage as the two oxidized cholesterol more than twice as much as the two oxidized cholesterol Any significant change in quality. Exogenous to the metallothionein can reduce cell damage, external to L-buthionein- [S, R] -sulfoximine cell damage increased, indicating damage and the content of sulfhydryl. The results suggest that oxidative cholesterol-induced cell damage may be through the generation of oxygen stress.