Jancsó Zsanett, Bódi Nikolett, Borsos Barbara, Fekete Éva, Hermesz Edit
Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary.
Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary.
Int J Biochem Cell Biol. 2015 May;62:125-31. doi: 10.1016/j.biocel.2015.03.005. Epub 2015 Mar 18.
The aim of this study was to seek possible links between the regionality along the digestive tract and the accumulation of reactive oxygen species, the effectiveness of the antioxidant defense system and the sensitivity to the types of demise in different gut regions of rats with streptozotocin-induced diabetes. Significant changes were observed in the oxidative status and in the activity of the antioxidant defense system in the diabetic colon; the peroxynitrite production was doubled, the level of hemoxygenase-2 protein was increased 11-fold and the expression of anti-apoptotic bcl-2 was also increased. The segment-specific vulnerability of the gastrointestinal tract induced by hyperglycemia was also confirmed by electron microscopy, demonstrating the presence of severe necrosis in the colon of the diabetic rats. No remarkable histopathological alterations were seen in the duodenum of the diabetic animals and there were likewise no significant changes in the production of peroxynitrite in their duodenum, whereas the level of the free radical scavenger metallothionein-2 was increased ∼300-fold.
The spatially restricted vulnerability observed along the digestive tract could originate from a high level of oxidative stress via peroxynitrite production.
本研究的目的是探寻链脲佐菌素诱导糖尿病大鼠不同肠道区域沿消化道的区域性与活性氧积累、抗氧化防御系统有效性以及对死亡类型的敏感性之间的可能联系。在糖尿病大鼠的结肠中，氧化状态和抗氧化防御系统活性出现显著变化；过氧亚硝酸盐生成量增加一倍，血红素加氧酶-2蛋白水平升高11倍，抗凋亡蛋白bcl-2的表达也增加。高血糖诱导的胃肠道节段特异性易损性也通过电子显微镜得到证实，显示糖尿病大鼠结肠存在严重坏死。糖尿病动物的十二指肠未见明显组织病理学改变，其十二指肠过氧亚硝酸盐生成也无显著变化，而自由基清除剂金属硫蛋白-2的水平增加了约300倍。
沿消化道观察到的空间受限易损性可能源于过氧亚硝酸盐生成导致的高水平氧化应激。
