Structural modifications of the prostate in hypoxia, oxidative stress, and chronic ischemia.
Structural modifications of the prostate in hypoxia, oxidative stress, and chronic ischemia.
复制标题
前列腺缺氧，氧化应激和慢性缺血的结构修饰。
DOI：
10.4111/kju.2015.56.3.187
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发表时间：
2015-03
期刊：
影响因子：
--
通讯作者：
Azadzoi KM
中科院分区：
文献类型：
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作者：
Thurmond P;Yang JH;Li Y;Lerner LB;Azadzoi KM
临床研究已经报道了老年男性盆腔缺血和排尿功能障碍之间的相关性。本研究的目的是确定和比较前列腺结构的修改，在培养的细胞和兔模型后暴露于缺氧，氧化应激和慢性缺血。培养的人前列腺平滑肌细胞（SMCs），上皮细胞（EC），和基质细胞（SC）下培养常氧，缺氧，和氧化应激条件下，通过使用计算机化的氧循环仪系统。我们建立了一个慢性前列腺缺血兔模型，通过建立髂动脉粥样硬化。采用荧光分析法和酶免疫分析法检测氧化应激标志物。用Masson三色染色和透射电镜观察前列腺结构。脂质过氧化被发现在SMCs暴露于缺氧和在所有类型的细胞暴露于氧化应激。我们确定了暴露于缺氧的EC和暴露于氧化应激的所有细胞类型中的蛋白质氧化。慢性缺血兔前列腺组织中存在指示氧化损伤的标记物。这些反应与DNA损伤有关。前列腺缺血导致上皮萎缩、平滑肌损失和弥漫性纤维化。TEM显示线粒体肿胀，嵴退化，膜丢失，高尔基体丢失，神经变性，细胞间连接中断。人前列腺细胞对缺氧和氧化应激表现出不同的反应，并伴有广泛的DNA损伤。缺血性前列腺组织中的结构改变与暴露于氧化应激的细胞中的结构改变相似。由于缺血和氧化应激引起的结构变化可能导致老年男性前列腺不依从。
Clinical studies have reported a correlation between pelvic ischemia and voiding dysfunction in elderly men. The aim of this study was to identify and compare prostate structural modifications in cultured cells and in a rabbit model after exposure to hypoxia, oxidative stress, and chronic ischemia. Cultured human prostate smooth muscle cells (SMCs), epithelial cells (ECs), and stromal cells (SCs) were incubated under normoxia, hypoxia, and oxidative stress conditions by use of a computerized oxycycler system. We developed a rabbit model of chronic prostate ischemia by creating aorto-iliac arterial atherosclerosis. Markers of oxidative stress were examined by using fluorometric analysis and enzyme immunoassay. Prostate structure was examined by using Masson's trichrome staining and transmission electron microscopy (TEM). Lipid peroxidation was found in SMCs exposed to hypoxia and in all cell types exposed to oxidative stress. We identified protein oxidation in ECs exposed to hypoxia and in all cell types exposed to oxidative stress. Markers indicating oxidative damage were present in chronically ischemic rabbit prostate tissue. These reactions were associated with DNA damage. Prostate ischemia resulted in epithelial atrophy, loss of smooth muscle, and diffuse fibrosis. TEM showed swollen mitochondria with degraded cristae, loss of membrane, loss of Golgi bodies, degenerated nerves, and disrupted cell-to-cell junctions. Human prostate cells exhibited differential reactions to hypoxia and oxidative stress with widespread DNA damage. Structural modifications in ischemic prostate tissue were similar to those in cells exposed to oxidative stress. Structural changes due to ischemia and oxidative stress may contribute to prostatic noncompliance in aging men.