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增生性玻璃体视网膜病变患者玻璃体中脂质过氧化物水平和髓过氧化物酶活性升高。

Increased lipid peroxide level and myeloperoxidase activity in the vitreous of patients suffering from proliferative vitreoretinopathy.

作者信息

Böker T, Augustin A J, Breipohl W, Spitznas M, Lutz J

机构信息

Department of Ophthalmology, University of Bonn, Germany.

出版信息

Graefes Arch Clin Exp Ophthalmol. 1994 Nov;232(11):652-6. doi: 10.1007/BF00171379.

Abstract

BACKGROUND

Retinal pigment epithelium cells and activated phagocytes are believed to be involved in the pathogenesis of proliferative vitreoretinopathy (PVR). Both cell types are capable of producing oxygen free radicals and other molecules with a high oxidative potential which can lead to a propagation of oxidative damage. It was the aim of this study to investigate whether products of oxidative reactions are detectable in the vitreous body of patients suffering from PVR.

METHODS

In vitreous aspirates of patients vitrectomized because of PVR (n = 27), macular pucker (n = 9), or other reasons (controls, n = 31), the following parameters were determined: lipid peroxides (LPO), determined as malondialdehyde-like substances (MDA) and as thiobarbituric acid-reactive substances (TBARS), and myeloperoxidase activity (MPO).

RESULTS

Compared with the controls, both LPO levels and MPO activities were significantly elevated in the vitreous of patients suffering from PVR. Vitreous of patients with macular pucker did not reveal any significant differences from controls in the parameters analyzed.

CONCLUSION

Our results suggest that both oxygen free radicals and inflammation-related reactions participate in the process of PVR. Oxidative tissue damage is obviously not involved in the pathogenesis of macular pucker.

摘要

背景

视网膜色素上皮细胞和活化的吞噬细胞被认为参与了增殖性玻璃体视网膜病变(PVR)的发病机制。这两种细胞类型都能够产生氧自由基和其他具有高氧化潜能的分子,这可能导致氧化损伤的扩散。本研究的目的是调查在患有PVR的患者的玻璃体中是否可检测到氧化反应产物。

方法

在因PVR(n = 27)、黄斑皱襞(n = 9)或其他原因(对照组,n = 31)而接受玻璃体切除术的患者的玻璃体抽吸物中,测定了以下参数:脂质过氧化物(LPO),以丙二醛样物质(MDA)和硫代巴比妥酸反应性物质(TBARS)来测定,以及髓过氧化物酶活性(MPO)。

结果

与对照组相比,患有PVR的患者玻璃体中的LPO水平和MPO活性均显著升高。黄斑皱襞患者的玻璃体在所分析的参数方面与对照组没有显示出任何显著差异。

结论

我们的结果表明,氧自由基和炎症相关反应均参与了PVR的过程。氧化组织损伤显然不参与黄斑皱襞的发病机制。

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