NO在甲醛介导的氧化损伤中的协同作用

为了探讨NO在甲醛介导的氧化损伤中的协同作用,用不同剂量的气态甲醛对小鼠进行连续动态染毒处理72 h后,测定小鼠脑、心和肝组织一氧化氮合酶活力和总抗氧化能力.结果显示,吸入甲醛后,小鼠的脑、心和肝组织一氧化氮合酶活力升高,总抗氧化能力下降.当甲醛浓度为0.5 mg·m-3时,脑和肝的一氧化氮合酶活力与阴性对照组相比有显著性差异(p＜0.05),脑和肝的总抗氧化能力与阴性对照组相比,有极显著性差异(p＜0.01),而心的总抗氧化能力与阴性对照组相比有显著性差异(p＜0.05).当甲醛浓度上升为3.0 mg·m-2时,脑、心和肝组织的一氧化氮合酶活力和总抗氧化能力与阴性对照组相比均有极显著性差异(p＜0.01).结果表明,过量生成的NO是甲醛导致机体氧化损伤可能的机理.

Study on coordinated effect of nitric oxide on oxidative damage induced by formaldehyde

To explore the coordinated effect of nitric oxide on oxidative damage induced by formaldehyde, the mice were treated with gaseous formaldehyde of different concentrations for 72 hours and the nitric oxide synthase activity and total antioxidant capacity of brain, heart and liver tissue were mensurated. The result shows that with formaldehyde concentration increasing, the nitric oxide synthase activity of brain, heart and liver tissue increases and total antioxidant capacity decreases in mice. Compared with the negative control, the nitric oxide synthase activity of brain and liver tissue increases(p<0.05) and total antioxidant capacity of brain and liver significantly decreases (p<0.01), while total antioxidant capacity of heart decreases (p<0.05) when concentration of formaldehyde is 0.5mg?m-3. The nitric oxide synthase activity of brain, heart and liver tissue significantly increases(p<0.05) and total antioxidant capacity significantly decreases (p<0.01) compared with the negative control when concentration of formaldehyde is 3.0mg?m-3. The result indicates that excessive nitric oxide may be the possible mechanism of oxidative damage induced by formaldehyde.