Lorentzon R, Boquist L
Virchows Arch B Cell Pathol Incl Mol Pathol. 1979;31(3):227-33. doi: 10.1007/BF02889939.
Using stereological techniques, including semi-automatic image analysis, the B-cell mitochondria were studied in the pancreatic islets from one group of control mice and two groups of mice killed 10 min and 60 min, respectively, after alloxan administration. Ten min following alloxan the mitochondrial volume and envelope surface densities, the mean mitochondrial volume and surface area, and the area of mitochondrial profiles were significantly increased, whereas the mitochondrial numerical density was not significantly altered. At the 60 min observation time the mitochondrial volume density, the mean mitochondrial volume and surface areas, and the area of mitochondrial profiles were significantly decreased, whereas the mitochondrial envelope surface was not significantly altered. The findings indicate a rapid swelling, followed by disintegration of the mitochondria in the B-cells of alloxan-treated mice, thereby supporting our view that mitochondrial lesions play a primary role in the development of alloxan diabetes. These lesions are believed to be due to ionic alterations in the B-cells ("Pi-pH hypothesis").
运用包括半自动图像分析在内的体视学技术,对一组对照小鼠以及分别在注射四氧嘧啶后10分钟和60分钟处死的两组小鼠胰岛中的B细胞线粒体进行了研究。四氧嘧啶注射10分钟后,线粒体体积和包膜表面密度、平均线粒体体积和表面积以及线粒体轮廓面积均显著增加,而线粒体数量密度未发生显著改变。在60分钟观察时间点,线粒体体积密度、平均线粒体体积和表面积以及线粒体轮廓面积均显著降低,而线粒体包膜表面未发生显著改变。这些发现表明,四氧嘧啶处理的小鼠B细胞中的线粒体迅速肿胀,随后解体,从而支持了我们的观点,即线粒体损伤在四氧嘧啶糖尿病的发展中起主要作用。这些损伤被认为是由于B细胞中的离子改变(“磷酸-氢离子假说”)所致。