Riede U N, Sandritter W, Pietzsch A, Rohrbach R
Pathol Res Pract. 1980 Dec;170(4):376-87. doi: 10.1016/S0344-0338(80)80042-2.
Under the influence of seven weeks of vitamin B6-free nutrition, the hepatocyte single volume is diminished in the face of an unchanged nuclear single volume, posing the question of whether there is proportional atrophy of all cell organelles or single organelle atrophy with counter-regulatory hyperplasia in other cellular compartments. The nucleoli hypertrophy, as the result of segregation and protein synthesis inhibition. The rough endoplasmic reticulum experiences hypoplasia, but the ultrastructural-morphometric analysis does not determine which metabolic steps are attacked. By contrast one observes hyperplasia in the smooth endoplasmic reticulum, which may be regarded as a counter-regulatory mechanism to the choking of protein synthesis. As with the rough endoplasmic reticulum, the mitochondria also show hypoplasia. This is due to the dependency of the mitochondria upon the endoplasmic protein synthesis. The disturbed functional output of the endoplasmic reticulum is seen in the reduced number of orthoperoxisomes as well. The Golgi apparatus experiences hypoplasia as a result of B6 hypovitaminosis, and this must be considered in the context of fatty change in the liver.
在七周无维生素B6营养的影响下,肝细胞单体积减小,而细胞核单体积不变,这就引发了一个问题:所有细胞器是否都存在比例性萎缩,还是单个细胞器萎缩而其他细胞区室存在反调节性增生。核仁肥大是分离和蛋白质合成抑制的结果。粗面内质网发育不全,但超微结构形态计量分析无法确定哪些代谢步骤受到了影响。相比之下,人们观察到滑面内质网增生,这可被视为对蛋白质合成受阻的一种反调节机制。与粗面内质网一样,线粒体也显示出发育不全。这是由于线粒体对内质网蛋白质合成的依赖性。内质网功能输出紊乱还表现为正过氧化物酶体数量减少。维生素B6缺乏症导致高尔基体发育不全,这在肝脏脂肪变性的背景下必须予以考虑。