论文部分内容阅读
给予大鼠吸入原油蒸气15g/m3×8h(急性染毒Ⅰ组)、30g/m3×8h(急性染毒Ⅱ组)、3g/m3×8h/d×30d(亚急性染毒组),观察血液和肺组织GSH、MDA含量和GSH-Px活性变化。结果3个染毒组大鼠血GSH含量均明显减少;肺GSH-Px活性均有所下降,尤以2个急性染毒组酶活性下降显著(P<0.01),急性染毒Ⅱ组大鼠肺GSH-Px活性仅约为对照组的1/3;急性染毒Ⅱ组大鼠肺MDA含量轻度增高,血MDA含量显著增高(P<0.05)。本研究提示原油蒸气吸入,可削弱机体氧自由基清除系统的抗脂质过氧化损伤的活性,并引起一定程度的生物膜脂质过氧化损伤。表明脂质过氧化损伤反应可能是原油蒸气吸入引起肺损伤的机理之一。
Rats were exposed to crude oil vapor 15g / m3 × 8h (acute exposure group Ⅰ), 30g / m3 × 8h (acute exposure group Ⅱ), 3g / m3 × 8h / d × 30d Blood and lung tissue GSH, MDA content and GSH-Px activity changes. Results The levels of GSH in the three exposure groups were significantly decreased. The activity of GSH-Px in the lung decreased, especially in the two acute exposure groups (P <0.01). In the acute exposure group Ⅱ The activity of GSH-Px in rat lung was only about 1/3 of that in the control group. The content of MDA in the lung of the rats in the acute exposure group was slightly increased, and the MDA content in the blood was significantly increased (P <0.05). This study suggests that crude vapor inhalation can weaken the antioxidant activity of the oxygen free radical scavenging system of the body and cause some degree of lipid peroxidation damage to the biofilm. It is suggested that lipid peroxidation injury may be one of the mechanisms of lung injury induced by crude vapor inhalation.