亚砷酸钠对雄性大鼠肺氧化损伤作用研究

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目的探讨亚砷酸钠(NaAsO_2)经饮水染毒对大鼠肺氧化损伤作用。方法无特定病原体级健康成年雄性SD大鼠,随机分为对照组和低、中、高剂量组,每组8只。3个剂量组大鼠自由饮用质量浓度分别为10.00、100.00和1 000.00μg/L的NaAsO_2溶液,对照组大鼠自由饮用超纯水。染毒28 d后处死大鼠,测定支气管肺泡灌洗液(BALF)中白细胞总数和细胞死亡率,以酶联免疫吸附实验测定BALF中活性氧(ROS)、还原型辅酶Ⅱ(NADPH)、总抗氧化能力和一氧化氮(NO)水平。结果中剂量组大鼠BALF中白细胞总数分别高于对照组和高剂量组(P<0.05);高剂量组大鼠BALF中细胞死亡率分别高于对照组、低剂量组和中剂量组(P<0.01)。低、中和高剂量组大鼠BALF中ROS水平分别高于对照组(P<0.01);中、高剂量组大鼠BALF中NADPH水平分别高于对照组和低剂量组(P<0.05);中和高剂量组大鼠BALF中总抗氧化能力分别低于对照组(P<0.01),但NO水平均高于对照组(P<0.05)。结论砷进入大鼠体内后可能是通过激活氧化酶NADPH使ROS高表达,进而使NO增多,造成组织氧化应激损伤。 Objective To investigate the effects of sodium arsenite (NaAsO_2) on lung injury induced by drinking water in rats. Methods Healthy male SD rats without specific pathogen were randomly divided into control group and low, medium and high dose groups, 8 in each group. Rats in the three dosage groups were given free NaAsO 2 solution of 10.00, 100.00 and 1000.00 μg / L, respectively. Rats in the control group were free to drink ultrapure water. The rats were sacrificed 28 days after exposure and the total number of white blood cells and cell death in BALF were measured. The levels of reactive oxygen species (ROS) Antioxidant capacity and nitric oxide (NO) levels. Results The total number of leukocytes in BALF in middle-dose group was higher than that in control group and high-dose group (P <0.05). The cell death rate of BALF in high-dose group was higher than that in control group, low-dose group and middle-dose group <0.01). The levels of ROS in BALF in low, middle and high dose groups were higher than those in control group (P <0.01). The levels of NADPH in BALF in middle and high dose groups were higher than those in control group and low dose group (P <0.05), respectively. The total antioxidant capacity of BALF in rats in middle and high dose groups was lower than that in control group (P <0.01), but the level of NO in BALF was higher than that in control group (P <0.05). Conclusion Arsenic may enter into the body of rats by activating the oxidase NADPH to make the high expression of ROS, thus increasing the NO, resulting in tissue oxidative stress injury.
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