Temneanu O R, Zamfir C, Eloaie Zugun F, Cojocaru E, Tocan L
Department of Histology, Gr. T. Popa University of Medicine and Pharmacy, Iasi, Romania.
J Med Life. 2011 Aug 15;4(3):244-9. Epub 2011 Aug 25.
Even if the reactive oxygen species were discovered, described and detailed a long time ago, there is still little data about the mechanisms of oxidative stress, their tissular effects and about an efficient antioxidant strategy, involving animal experimental models. It has been shown that the lung is one of the most exposed organs to the oxidative stress. The particular effects of different types of oxidative stress on lungs were investigated in this experimental study, in order to quantify the intensity and the extent of the pulmonary damage, featuring the antioxidant enzymatic protective role.
The study of lung injury was performed on four distinct groups of Wistar rats: a control group versus a group exposed to continuous light deprivation versus a group exposed to nitrofurantoin versus a group exposed to continuous light deprivation, to nitrofurantoin and vitamin C. Pulmonary samples were taken and treated for microscopic analysis. A qualitative immunohistochemical estimation of pulmonary superoxide dismutase 1 (SOD 1) was performed. Blood tests were used in order to reveal the presence and intensity of oxidative stress.
Continuous light deprivation and the chronic administration of nitrofurantoin acted as oxidants with a certain involvement in lung damage--vascular and alveolar wall disturbances. Adding an antioxidant, such as vitamin C, considerably improved lung reactivity to oxidative stress.
The chronic exposure to oxidants in the induced oxidative stress sustains the development of specific lung alterations. SOD 1 positive reaction underlines the complex enzymatic defense in oxidative stress.
即使活性氧早在很久以前就已被发现、描述和详细研究，但关于氧化应激机制、其组织效应以及涉及动物实验模型的有效抗氧化策略的数据仍然很少。研究表明，肺是最易受到氧化应激影响的器官之一。本实验研究调查了不同类型氧化应激对肺的特定影响，以量化肺损伤的强度和程度，突出抗氧化酶的保护作用。
对四组不同的Wistar大鼠进行肺损伤研究：一组为对照组，一组暴露于持续光照剥夺环境，一组暴露于呋喃妥因，一组暴露于持续光照剥夺环境并同时给予呋喃妥因和维生素C。采集肺组织样本并进行处理以进行显微镜分析。对肺超氧化物歧化酶1（SOD 1）进行定性免疫组织化学评估。进行血液检测以揭示氧化应激的存在和强度。
持续光照剥夺和长期给予呋喃妥因作为氧化剂，在一定程度上参与了肺损伤——血管和肺泡壁紊乱。添加抗氧化剂，如维生素C，可显著改善肺对氧化应激的反应性。
在诱导的氧化应激中慢性暴露于氧化剂会促进特定肺改变的发展。SOD 1阳性反应突出了氧化应激中复杂的酶防御作用。
