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目的 探讨烹调油烟（ＣＯＦ） 致肺损伤及毒作用机理。方法 利用ＳＤ 大鼠动式吸入烹调油烟［（４３ ±４）ｍｇ／ｍ３］ 制备动物模型，分三个时相（２０ 、４０ 、６０ ｄ） 观察ＣＯＦ 对肺脏Ｓ９ 中ＳＯＤ 活性，ＭＤＡ 和微量元素Ｚｎ 、Ｃｕ 、Ｆｅ 含量及组织病理学变化。结果 ＣＯＦ可使肺组织ＭＤＡ 含量增多，ＳＯＤ 酶活性下降；Ｚｎ 、Ｃｕ、Ｆｅ 代谢紊乱，以吸入ＣＯＦ６０ 天改变最明显；肺组织出现不典型增生等癌前病变。结论 长期吸入ＣＯＦ引起肺脂质过氧化和微量元素紊乱可能与肺损伤及其癌前病变存在一定的联系。
Objective To investigate the lung injury induced by cooking fume (COF) and its toxic mechanism. Methods Animal model was established by inhalation of soot in rats [(43 ± 4) mg / m 3], and the effects of COF on SOD, MDA and trace elements in lung S9 were observed in three phases (20, 40 and 60 d) Zn, Cu, Fe content and histopathological changes. Results COF increased the content of MDA and decreased the activity of SOD in lung tissue. The metabolism of Zn, Cu and Fe was disordered. COF was the most obvious change in 60 days and the atypical hyperplasia and other precancerous lesions in lung tissue. Conclusion Long-term COF inhalation induced pulmonary lipid peroxidation and trace element disorders may be related to lung injury and precancerous lesions.