Montgomery M R, Teuscher F, LaSota I, Niewoehner D E
J Environ Pathol Toxicol Oncol. 1986 Sep-Dec;7(1-2):169-80.
Groups of male rats were exposed to acute doses of oxygen, ozone, or paraquat which produced equivalent mortality (25-30%) over a 28 day post-exposure period. Quantitative evaluation of morphological changes indicated the primary response to be edema and inflammation with only slight fibrosis being apparent by the end of the observation period. Aerobic pulmonary metabolism was inhibited in lungs from animals exposed to oxygen and ozone as evidenced by decreased oxygen consumption; however, this was transient and O2 consumption returned to normal within 24 hours after removal from the exposure chamber. Conversely, treatment with paraquat caused an immediate, transient stimulation of O2 consumption. Glucose metabolism was unaltered by the gas exposures and, as previously reported, was initially stimulated by paraquat treatment. In vitro, only paraquat altered both O2 consumption and glucose metabolism when added to lung slice preparations; ozone had no effect. Oxygen did not alter O2 consumption but caused a slight biphasic response in glucose metabolism. Aerobic metabolism is relatively unchanged by these doses of oxygen and ozone which result in the death of 25-30% of all treated animals. Even though paraquat produces similar morphologic changes, it may represent a more severe metabolic insult than "equivalent" doses of oxygen or ozone. Also, if interstitial pulmonary fibrosis is a desired result of experimental exposure, rats may not be a suitable model for oxidant induced lung injury.
将雄性大鼠分组,使其暴露于急性剂量的氧气、臭氧或百草枯中,在暴露后的28天内,这些物质导致的死亡率相当(25%-30%)。形态学变化的定量评估表明,主要反应是水肿和炎症,在观察期结束时仅有轻微纤维化。暴露于氧气和臭氧的动物肺部的需氧肺代谢受到抑制,这可通过氧气消耗减少得到证明;然而,这是短暂的,从暴露室移出后24小时内氧气消耗恢复正常。相反,百草枯处理导致氧气消耗立即出现短暂刺激。气体暴露对葡萄糖代谢没有影响,如先前报道,百草枯处理最初会刺激葡萄糖代谢。在体外,当添加到肺切片制剂中时,只有百草枯改变了氧气消耗和葡萄糖代谢;臭氧没有影响。氧气没有改变氧气消耗,但在葡萄糖代谢中引起了轻微的双相反应。这些剂量的氧气和臭氧导致所有处理动物中有25%-30%死亡,但对需氧代谢的影响相对较小。尽管百草枯产生类似的形态学变化,但它可能比“等效”剂量的氧气或臭氧代表更严重的代谢损伤。此外,如果实验性暴露期望产生间质性肺纤维化,大鼠可能不是氧化应激诱导肺损伤的合适模型。