WILSON J W, LEDUC E H
J Cell Biol. 1963 Feb;16(2):281-96. doi: 10.1083/jcb.16.2.281.
Livers of mice on diets deficient in essential fatty acids (EFA) have been studied by light and electron microscopy. The most conspicuous changes occur in the mitochondria. In light microscopy the mitochondria appear very much enlarged in the periportal region of the lobule. In electron micrographs they have additional cristae, sometimes very abundant. ranged in stacks in the central cavity. The matrix may be more electron-opaque than normal. This is in contrast with the enlarged mitochondria appearing under other experimental conditions, where the cristae are reduced in number and the matrix is less electron-opaque. It is known that there is an uncoupling of oxidative phosphorylation in EFA-deficient mitochondria. As a hypothesis it is proposed that the uncoupling may be due to a molecular defect caused by the absence of EFA in the structure that determines the spatial relationship between the electron transport chain and oxidative phosphorylation. It is further tentatively suggested that the changes in mitochondria may be attributed to lack of ATP. The possibility is discussed that the mitochondrial changes are ineffective attempts at compensation for this lack.
通过光学显微镜和电子显微镜对缺乏必需脂肪酸（EFA）饮食的小鼠肝脏进行了研究。最明显的变化发生在线粒体中。在光学显微镜下，小叶门周区域的线粒体显得非常大。在电子显微镜照片中，它们有额外的嵴，有时非常丰富，排列在中央腔内的堆叠中。基质可能比正常情况下更具电子不透明性。这与在其他实验条件下出现的肿大线粒体形成对比，在其他条件下嵴的数量减少且基质的电子不透明性较低。已知在缺乏EFA的线粒体中氧化磷酸化发生解偶联。作为一种假设，有人提出这种解偶联可能是由于在决定电子传递链与氧化磷酸化之间空间关系的结构中缺乏EFA而导致的分子缺陷。进一步初步认为线粒体的变化可能归因于ATP的缺乏。讨论了线粒体变化可能是对这种缺乏进行补偿的无效尝试的可能性。
