Rodvien R, Tavassoli M, Crosby W H
Am J Pathol. 1974 May;75(2):243-54.
Splenic ultrastructure was studied in experimentally induced severe iron deficiency in rabbits. Fragmentation and phagocytosis of blood cells, particularly red cells and platelets, were observed in the red pulp. Mitochondrial changes similar to those previously described in other sideropenic tissues were noted in the lympholytes and reticular cells of both the red and white pulp. The most striking findings were the changes associated with the membranous structures and endoplasmic reticulum. These changes were similar to those characteristically associated with lipid peroxidation. Glutathione peroxidase was shown to be deficient in the red cells of these sideropenic animals. The morphologic changes observed may be explained on the basis of lipid peroxidation of membranes, and it is suggested that iron deficiency results in "deficiency" of enzymes normally responsible for the protection of tissues against peroxidation injury. Increased susceptibility to peroxides may lead to peroxidation injury of membranous structures and morphologic changes described herein.
在实验诱导的兔严重缺铁模型中，对脾脏超微结构进行了研究。在脾红髓中观察到血细胞，特别是红细胞和血小板的破碎及吞噬现象。在红髓和白髓的淋巴细胞及网状细胞中，发现了与先前在其他缺铁性组织中所描述的类似的线粒体变化。最显著的发现是与膜结构和内质网相关的变化。这些变化类似于典型的脂质过氧化相关变化。研究表明，这些缺铁动物的红细胞中谷胱甘肽过氧化物酶缺乏。观察到的形态学变化可能基于膜的脂质过氧化来解释，并且提示缺铁导致通常负责保护组织免受过氧化损伤的酶“缺乏”。对过氧化物敏感性增加可能导致膜结构的过氧化损伤及本文所述的形态学变化。
