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缺血性视网膜中过氧化氢的产生:高血糖和缺血后氧张力的影响

Hydrogen peroxide production in ischaemic retina: influence of hyperglycaemia and postischaemic oxygen tension.

作者信息

Zhang H, Agardh E, Agardh C D

机构信息

Laboratory for Experimental Brain Research, University of Lund, Sweden.

出版信息

Diabetes Res. 1991 Jan;16(1):29-35.

PMID:1818795
Abstract

Free radicals have recently been proposed to play a role in the development of diabetic retinopathy. Ischaemia and hyperglycaemia followed by recirculation have been suggested to initiate free radical production in other tissues and the aim of the present study was to examine whether this could also be the case in the retina. The present study showed retinal cell damage, as measured by pycnotic cells, to be more pronounced when ischaemia was combined with hyperglycaemia than when combined with normoglycaemia. As an indication of free radical production, catalase activity was measured, reflecting the production of hydrogen peroxide (H2O2). Small amounts of H2O2 were found to be generated in the normal retina, but did not increase during ischaemia and hyperglycaemia followed by recirculation. It thus seems, as if hyperglycaemia aggravates the harmful effects of ischaemia, but with the methods used, there does not seem to be any increase in free radical production (as measured by H2O2 production) in normal rat retina during ischaemic and hyperglycaemic conditions.

摘要

最近有人提出自由基在糖尿病视网膜病变的发展中起作用。缺血和高血糖继以再灌注已被认为会引发其他组织中的自由基产生,而本研究的目的是检验视网膜是否也是这种情况。本研究显示,以固缩细胞衡量的视网膜细胞损伤,在缺血与高血糖合并时比与正常血糖合并时更明显。作为自由基产生的一个指标,测定了过氧化氢酶活性,反映过氧化氢(H2O2)的产生。在正常视网膜中发现有少量H2O2产生,但在缺血、高血糖继以再灌注过程中并未增加。因此似乎高血糖会加重缺血的有害影响,但就所使用的方法而言,在缺血和高血糖状态下,正常大鼠视网膜中似乎没有自由基产生增加(以H2O2产生衡量)的情况。

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