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为研究过量三氧化二砷(arsenic trioxide,ATO)摄入对小鼠脾氧化应激和甲硫氨酸亚砜还原酶基因表达的影响,将30只6周龄雄性小鼠随机分成6组,每组分别连续3周口服不同剂量三氧化二砷(按体重0、0.3、1、3、6、9mg/kg),然后分析小鼠脾氧化应激状态和甲硫氨酸亚砜还原酶基因表达的变化。结果显示,不同剂量的ATO处理均导致小鼠脾膜脂过氧化加剧(P<0.01),也导致总超氧化物歧化酶(SOD)活性显著下降(P<0.01),各处理组间无显著差异。qPCR分析显示,不同剂量ATO处理诱导了MsrA和MsrB2基因表达的显著上升,高剂量ATO上调了MsrB1基因的表达,但抑制了小鼠脾中MsrB3基因的表达。结果表明,ATO的摄入导致了小鼠脾膜脂过氧化并降低了SOD活性,MsrA、MsrB1和MsrB2基因可能在减轻ATO导致的小鼠脾蛋白氧化修复中起重要作用。
In order to study the effect of excessive intake of arsenic trioxide (ATO) on splenic oxidative stress and methionine sulfoxide reductase gene expression in mice, 30 6-week-old male mice were randomly divided into 6 groups, each group Three different doses of arsenic trioxide (0, 0.3, 1, 3, 6 and 9 mg / kg) were orally administered orally for 3 consecutive weeks. The changes of splenic oxidative stress and methionine sulfoxide reductase gene expression in mice were analyzed. The results showed that ATO treatment at different dosages resulted in an increase of splenic lipid peroxidation (P <0.01) and a significant decrease of total superoxide dismutase (SOD) activity (P <0.01) difference. qPCR analysis showed that different doses of ATO treatment induced a significant increase of MsrA and MsrB2 gene expression, while high dose of ATO up-regulated MsrB1 gene expression, but suppressed MsrB3 gene expression in mouse spleen. The results showed that ATO uptake led to the spleen lipid peroxidation and decreased the activity of SOD in mice. The MsrA, MsrB1 and MsrB2 genes may play an important role in alleviating ATO-induced oxidative repair of splenic mice.