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首页> 外文期刊>Biological trace element research >Effect of selenomethionine supplementation in food on the excretion and toxicity of arsenic exposure in female mice
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Effect of selenomethionine supplementation in food on the excretion and toxicity of arsenic exposure in female mice

机译:食物中添加硒代蛋氨酸对雌性小鼠砷暴露的排泄和毒性的影响

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摘要

Selenium (Se) is an essential component of several major metabolic pathways and controls immune function. Arsenic (As) is a human carcinogen with immunotoxic and genotoxic activities, functioning mainly by producing oxidative stress. Due to the ability of Se to interact with As and to possibly block its toxic effects, we investigated the impact of dietary Se-methionine (Se-Met) supplementation on the toxicity of As exposure in vivo in a mouse model. Sufficient and excess levels of Se-Met (0.2 and 2 ppm, respectively) were fed to C57BL/6N female mice exposed to sodium arsenite (3, 6 and 10 mg/kg) in tap water for 9 days. We observed that As exposure increased Se-Met excretion in the urine. Se-Met supplementation increased the relative liver weight and decreased the concentration of total liver proteins in animals exposed to 10 mg/kg of As. Se-Met supplementation maintained a normal pool of glutathione in the liver and increased glutathione peroxidase concentration, although the lipoperoxidation level was increased by Se-Met even without As exposure. Se-Met supplementation helped to maintain the CD4/CD8 ratio of lymphocytes in the spleen, although it increased the proportion of B cells. Se-Met supplementation prior to As exposure increased the secretion of interleukin-4, IL-12 and interferon-γ and the stimulation index of the spleen cells in in vitro assays. Se-Met intake improved the basal immunological parameters but did not reduce the damage caused by oxidative stress after low-dose As exposure.
机译:硒(Se)是几种主要代谢途径的重要组成部分,并控制免疫功能。砷(As)是具有免疫毒性和遗传毒性活性的人类致癌物,主要通过产生氧化应激而起作用。由于Se与As相互作用并可能阻断其毒性作用的能力,我们在小鼠模型中研究了日粮添加Se-蛋氨酸(Se-Met)对As暴露于体内的毒性的影响。将Se-Met的过量和过量(分别为0.2和2 ppm)喂给在自来水中暴露于亚砷酸钠(3、6和10 mg / kg)的C57BL / 6N雌性小鼠9天。我们观察到,As暴露会增加尿中Se-Met的排泄。 Se-Met补充剂增加了暴露于10 mg / kg As的动物的相对肝脏重量,并降低了总肝蛋白浓度。 Se-Met补充剂可维持肝脏中正常的谷胱甘肽库并增加谷胱甘肽过氧化物酶浓度,尽管即使没有As暴露,Se-Met也会增加脂过氧化水平。 Se-Met补充剂虽然可以增加B细胞的比例,但有助于维持脾脏淋巴细胞CD4 / CD8的比例。在体外试验中,As暴露前补充Se-Met可增加白细胞介素4,IL-12和干扰素-γ的分泌以及脾细胞的刺激指数。 Se-Met摄入改善了基础免疫学参数,但没有减少低剂量As暴露后由氧化应激引起的损害。

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