Anderson W R, Tan W C, Takatori T, Privett O S
Arch Pathol Lab Med. 1976 Mar;100(3):154-62.
Intravenous administration of methyl linoleate hydroperoxide (MLH) uniformly resulted in extensive damage to septal wall components of the rat lung; the severity of these changes paralleled the administered dosage. The target cell of injury appeared to be the capillary endothelial cell. Destructive changes within the plasma membrane suggested that the major toxic effect of MLH was directed against membranous structures. Ultrastructural analysis showed that these effects were more severe in the vitamin E-deficient animals. Secondary changes were characterized by interstitial and alveolar edema, and degenerative changes within alveolar pneumocytes. Reparative proliferation of type 2 pneumocytes first became evident in animals that survived two days. These observations provide an insight into the susceptibility and sequential damage to pulmonary tissue by hydroperoxides and serve as a guide for investigations of the toxic effects of other oxidants on lung.
静脉注射亚油酸氢过氧化物(MLH)均会对大鼠肺脏的间隔壁成分造成广泛损伤;这些变化的严重程度与给药剂量平行。损伤的靶细胞似乎是毛细血管内皮细胞。质膜内的破坏性变化表明,MLH的主要毒性作用针对膜结构。超微结构分析表明,这些影响在维生素E缺乏的动物中更为严重。继发性变化的特征是间质和肺泡水肿,以及肺泡上皮细胞的退行性变化。存活两天的动物中,Ⅱ型肺泡上皮细胞的修复性增殖首先变得明显。这些观察结果有助于深入了解氢过氧化物对肺组织的易感性和顺序性损伤,并为研究其他氧化剂对肺的毒性作用提供指导。