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砷暴露或过量吸收能导致多种疾病和病理损伤。本文旨在研究三氧化二砷(As_2O_3)暴露对小鼠肾氧化应激与甲硫氨酸亚砜还原酶基因表达的影响。对6周龄雄性小鼠分别用不同剂量(0、0.3、1.0、3.0、6.0、9.0 mg/kg)As_2O_3进行连续3周颈部皮下注射处理,然后分析小鼠肾脂质过氧化产物丙二醛(malondialdehyde,MDA)质量摩尔浓度、超氧化物歧化酶(superoxide dismutase,SOD)比活性和4种甲硫氨酸亚砜还原酶(methionine sulfoxide reductase,Msr)基因Msr A、Msr B1、Msr B2、Msr B3表达情况的变化。结果显示,不同剂量As_2O_3处理对小鼠肾膜脂过氧化水平没有显著影响;As_2O_3诱导了SOD比活性的增加,但9.0 mg/kg剂量组SOD比活性显著降低;不同Msr基因对As_2O_3表现出差异性反应,Msr A、Msr B3基因表达不受影响,As_2O_3处理后Msr B1基因的表达显著下调,而高剂量的As_2O_3则显著上调了Msr B2基因的表达。结果表明,9.0 mg/kg以下的As_2O_3暴露对小鼠肾膜脂过氧化影响不大,但明显诱导了SOD比活性的上升,Msr B2基因在小鼠肾适应As_2O_3暴露中发挥了重要作用。
Arsenic exposure or excessive absorption can lead to a variety of diseases and pathological damage. The aim of this study was to investigate the effects of arsenic trioxide (As 2 O 3) exposure on oxidative stress in mice and methionine sulfoxide reductase gene expression. Male 6-week-old mice were treated with different doses (0,0.3,1.0,3.0,6.0,9.0 mg / kg) of As_2O_3 for 3 consecutive weeks, respectively, and then subcutaneously injected into the neck of mice. The mass concentration of malondialdehyde (MDA), the specific activity of superoxide dismutase (SOD) and the activity of four methionine sulfoxide reductase (Msr) genes Msr A, Msr B1 and Msr B2 , Msr B3 expression changes. The results showed that As 2 O 3 treatment had no significant effect on the level of renal peritoneal lipid peroxidation in mice; As 2 O 3 induced the increase of specific activity of SOD, but the activity of SOD in 9.0 mg / kg dose group was significantly lower than that of As 2 O 3; The Msr B3 gene expression was not affected. The Msr B1 gene expression was significantly down-regulated after treated with As 2 O 3, while the high dose As 2 O 3 significantly up-regulated the Msr B2 gene expression. The results showed that exposure to As_2O_3 below 9.0 mg / kg had little effect on the peritoneal membrane lipid peroxidation in mice, but significantly increased the specific activity of SOD. The Msr B2 gene played an important role in the adaptation of As_2O_3 in mice kidney.