Protective Role of Selenium Against Hemolytic Anemia Is Mediated Through Redox Modulation
Protective Role of Selenium Against Hemolytic Anemia Is Mediated Through Redox Modulation
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DOI：
10.1007/s12011-018-1483-y
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发表时间：
2019-06-01
影响因子：
3.9
通讯作者：
Kaushal, Naveen
中科院分区：
文献类型：
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作者：
Kaur, Rankaljeet;Ghanghas, Preety;Kaushal, Naveen
硒（Se）是人体必需的微量元素和营养性抗氧化剂，通过与谷胱甘肽过氧化物酶（GPx）等硒蛋白结合而发挥其生物学效应。GPx水平的适度降低可能是红细胞过氧化的部分原因，这导致溶血性贫血。因此，膳食硒作为硒蛋白（GPx），可能通过阻止氧化应激介导的溶血来维持红细胞内稳态，调节红细胞生成。用酵母饲料喂养Balb/c小鼠8周，建立低硒（0.01ppm）、适硒（0.1ppm亚硒酸钠）和补硒（0.5ppm亚硒酸钠）状态，通过测定血浆硒水平和硒依赖性硒蛋白的活性和表达，建立低硒（0.01ppm）、适硒（0.1ppm亚硒酸钠）和补硒（0.5ppm亚硒酸钠）状态。各组小鼠腹腔注射苯肼（PHZ，20 mg/kg），每只小鼠50%。导致溶血性贫血结果表明，PHZ处理的硒缺乏动物表现出溶血增加，红细胞形态异常，海因茨小体和网织红细胞增加，血红蛋白变性为珠蛋白沉淀物和高铁血红蛋白。硒补充保护这些溶血性变化，使红细胞不那么脆弱。这些发现是一致的饮食硒浓度依赖性变化的活动和表达的GPx表明ROS介导的氧化应激是不可或缺的溶血。硒补充剂对增加水平的ROS，蛋白质羰基，和过氧化损伤膜脂质和酶的抗氧化剂的保护作用验证了这些观察。总之，膳食硒补充剂保护红细胞对溶血减轻ROS介导的氧化应激。
Selenium (Se), an essential trace element and potent nutritional antioxidant, exerts its biological effects through incorporation into selenoproteins like glutathione peroxidase (GPx). Modest decrement in the levels of GPx could be partly responsible for peroxidation of RBCs, which results into hemolytic anemia. Therefore, it is hypothesized that dietary Se, as selenoproteins (GPx), can maintain the homeostasis in RBCs and regulate the erythropoiesis by preventing oxidative stress-mediated hemolysis. Se-deficient (0.01ppm), Se-adequate (0.1ppm sodium selenite), and Se-supplemented (0.5ppm sodium selenite) status were created in Balb/c mice by feeding yeast-based diets for 8weeks and established by measuring Se levels in plasma and activities, expressions of Se-dependent selenoproteins. Fifty percent of mice from each differential Se group were treated with phenylhydrazine (PHZ, 20mg/kg, i.p.) to induce hemolytic anemia. Results indicated that PHZ-treated Se-deficient animals demonstrated increased hemolysis, abnormal RBC morphology, increase in Heinz bodies and reticulocytes, and denaturation of hemoglobin to globin precipitates and methemoglobin. Se supplementation protected against these hemolytic changes and makes RBCs less fragile. These findings were consistent with dietary Se concentration-dependent changes in activity and expression of GPx indicating that ROS-mediated oxidative stress is integral to hemolysis. Protective effects of Se supplementation against increased levels of ROS, protein carbonyls, and peroxide damage to membrane lipids and enzymatic antioxidants validated these observations. In conclusion, dietary Se supplementation protected the RBCs against hemolysis by mitigating ROS-mediated oxidative stress.