Redox changes precede the occurrence of oxidative stress in eyes and aorta, but not in kidneys of diabetic rats.
Redox changes precede the occurrence of oxidative stress in eyes and aorta, but not in kidneys of diabetic rats.
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DOI：
10.1016/s0024-3205(03)00662-3
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发表时间：
2003-10
期刊：
影响因子：
6.1
通讯作者：
K. Yue;Wai-shing Chung;Albert Wingnang Leung;C. H. Cheng
中科院分区：
文献类型：
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作者：
K. Yue;Wai-shing Chung;Albert Wingnang Leung;C. H. Cheng
几乎所有的糖尿病并发症都与不同组织的血管功能障碍有关。另一方面，氧化应激与糖尿病的发病机制有关。因此，在本研究中，我们研究了氧化还原状态和氧化应激在眼睛，主动脉和肾脏的链脲佐菌素（STZ）诱导的糖尿病大鼠之间的相关性。在STZ注射后的不同时间点，测量糖尿病大鼠这些组织中主要内源性抗氧化剂谷胱甘肽（GSH）和氧化应激标志物丙二醛（MDA）。我们的研究结果表明，GSH显着减少，在两个糖尿病大鼠眼和主动脉STZ注射后8周（43%和66%，分别为对照组）。此外，从STZ注射后第一周开始出现GSH耗竭，与对照组大鼠相比，GSH水平仍然较低（第1周和第8周：眼睛和主动脉中分别为对照组的43%和66%）。直到注射STZ后第8周，MDA才增加（眼睛和主动脉分别为对照组的177%和93%）。然而，在肾脏中未发现这些变化，其中GSH略有增加，MDA保持与对照大鼠相当。这些结果表明不同的组织对高糖条件的反应不同，因为氧化还原变化和氧化应激仅发生在糖尿病大鼠的眼睛和主动脉中，而不是在肾脏中。此外，氧化应激的发生之前，谷胱甘肽的消耗和可能的抗氧化防御系统的耗尽。此外，维生素E的管理被发现正常的MDA水平在眼睛和主动脉，但不是在糖尿病大鼠的肾脏。总之，我们的研究结果表明，在眼睛和主动脉中发展糖尿病并发症的潜在机制涉及氧化应激的发生，这可能不是糖尿病肾脏的情况。此外，维生素E可以通过减少细胞中的脂质过氧化和氧化损伤来预防眼睛和主动脉中糖尿病并发症的发展。
Almost all diabetic complications are known to be associated with vascular dysfunctions of different tissues. Oxidative stress, on the other hand, has been implicated in the pathogenesis of diabetes mellitus. Therefore in the present study we have investigated the correlation between redox status and oxidative stress in the eyes, aorta and kidneys of streptozotocin (STZ)-induced diabetic rats. Glutathione (GSH), the primary endogenous antioxidant, and malondialdehyde (MDA), a marker of oxidative stress, were measured in these tissues of diabetic rats at different time points after STZ injection. Our results showed that GSH was reduced significantly in both the eyes and aorta of diabetic rats 8 weeks after STZ injection (43% and 66% of the control, respectively). Furthermore, the depletion of GSH occurred from the first week after STZ injection, and the level remained low as compared with the control rats (both week 1 and week 8: 43% and 66% of the control in the eyes and aorta, respectively). MDA was not increased until week 8 onwards after STZ-injection (177% and 93% of the control in the eyes and aorta, respectively). These changes, however, were not found in the kidneys, in which the GSH was slightly increased and MDA remained comparable to the control rats. These results indicate different tissues respond differently to high glucose conditions as redox changes and oxidative stress occurred only in the eyes and aorta but not in the kidneys of diabetic rats. In addition, the onset of oxidative stress is preceded by a depletion of GSH and probably an exhaustion of the antioxidant defense system. Furthermore, administration of Vitamin E was found to normalize MDA levels in the eyes and aorta but not in the kidneys of diabetic rats. In summary, our results suggest that the underlying mechanism in developing diabetic complications in the eyes and aorta involves the occurrence of oxidative stress, which may not be the case in diabetic kidneys. In addition, Vitamin E may prevent the development of diabetic complications in the eyes and aorta by reducing lipid peroxidation and oxidative damage in the cells.