Azeez Oyebisi M, Akhigbe Roland E, Anigbogu Chikodi N
Department of Veterinary Physiology and Pharmacology, Faculty of Veterinary Medicine, University of Ilorin, Ilorin, Kwara state, Nigeria.
Toxicol Int. 2012 Sep;19(3):306-9. doi: 10.4103/0971-6580.103678.
Various studies have implicated automobile exhausts as risk factors in cardiovascular and pulmonary diseases; however, there is little or no documentation on the role of the main source of the exhausts, petroleum hydrocarbons, on cardiopulmonary pathologies. Thus, we investigated the effect of petroleum hydrocarbons, using various petroleum products, on histomorphology of the lung and the role of lipid peroxidation in it.
Control rats were not exposed to any of the petroleum products, whereas petrol-exposed, diesel-exposed, and kerosene-exposed rats were exposed to petrol, diesel, and kerosene by inhalation, respectively.
Exposure to petroleum hydrocarbons significantly induced lipid peroxidation with a consequent rise in malondialdehyde (MDA), and a decrease in superoxide dismutase (SOD) and catalase (CAT) activities and glutathione (GSH) level. Exposure to petroleum hydrocarbons also caused an alteration in the histomorphology of lung tissues.
Our findings imply that exposure to petroleum hydrocarbons by inhalation is a risk factor in the pathophysiology of pulmonary dysfunction. This is associated with oxidative stress.
多项研究表明汽车尾气是心血管疾病和肺部疾病的风险因素；然而，关于尾气的主要来源——石油碳氢化合物对心肺病理的作用，几乎没有相关文献记载。因此，我们使用各种石油产品，研究了石油碳氢化合物对肺组织形态学的影响以及脂质过氧化在其中的作用。
对照组大鼠不接触任何石油产品，而汽油暴露组、柴油暴露组和煤油暴露组大鼠分别通过吸入方式接触汽油、柴油和煤油。
接触石油碳氢化合物显著诱导脂质过氧化，导致丙二醛（MDA）水平升高，超氧化物歧化酶（SOD）、过氧化氢酶（CAT）活性及谷胱甘肽（GSH）水平降低。接触石油碳氢化合物还导致肺组织的组织形态学发生改变。
我们的研究结果表明，吸入石油碳氢化合物是肺功能障碍病理生理学中的一个风险因素。这与氧化应激有关。
