Sell D A, Reynolds E S
J Cell Biol. 1969 Jun;41(3):736-52. doi: 10.1083/jcb.41.3.736.
Iodoform, a relatively water-insoluble yellow solid, chemically reactive in free-radical reactions, produces early hepatocellular injury qualitatively similar to that of carbon tetrachloride. 2 hr after administration of radioactively labeled iodoform, nonvolatile (14)C is preferentially recovered in microsomal lipid and protein. By 30 min microsomal properties are profoundly affected: oxidative demethylation decreases abruptly; increased lipoperoxide decomposition products are detected; and amino acid incorporation into liver protein is depressed. By 1 hr glucose-6-phosphatase is suppressed centrolobularly and increased stainable calcium is present in the midzone. Increased cell sap RNA contents are observed by 2 hr. Morphologically, the biochemical and histochemical changes are associated with progressive dispersion, vacuolation, and degranulation of the granular endoplasmic reticulum. Calcium-associated masses accumulate within the mitochondrial matrix, and mitochondria become progressively pleomorphic. Golgi components dilate and disperse. Membranous components of the cytoplasm of parenchymal cells conglomerate into labyrinthine tubular aggregates. Lipid accumulates in cytoplasmic droplets. Ultimately, centrolobular necrosis ensues. The close cytochemical and morphological similarities between the cellular injury produced in the liver by iodoform and that produced by carbon tetrachloride suggest common pathogenetic mechanisms associated with damage to membranes.
碘仿是一种相对难溶于水的黄色固体，在自由基反应中具有化学反应性，可产生与四氯化碳所致肝细胞损伤性质相似的早期肝细胞损伤。给予放射性标记的碘仿2小时后，非挥发性的（14）C优先在微粒体脂质和蛋白质中被回收。到30分钟时，微粒体性质受到深刻影响：氧化脱甲基作用突然降低；检测到脂质过氧化物分解产物增加；氨基酸掺入肝蛋白受到抑制。到1小时时，葡萄糖-6-磷酸酶在小叶中心受到抑制，中区可染色钙增加。2小时时观察到细胞液RNA含量增加。形态学上，生化和组织化学变化与颗粒内质网的逐渐分散、空泡化和脱颗粒有关。钙相关物质在线粒体基质内积聚，线粒体逐渐出现多形性。高尔基体成分扩张并分散。实质细胞胞质的膜性成分聚集成迷宫样管状聚集体。脂质积聚在胞质小滴中。最终，小叶中心坏死发生。碘仿和四氯化碳在肝脏中产生的细胞损伤之间密切的细胞化学和形态学相似性表明，存在与膜损伤相关的共同发病机制。
