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带3/阴离子交换蛋白1/溶质载体家族4成员1的表达作为细胞对亚硒酸盐暴露敏感性的决定因素。

Band 3/anion exchanger 1/solute carrier family 4 member 1 expression as determinant of cellular sensitivity to selenite exposure.

作者信息

Fukumoto Yasunori, Matsuhashi Kemmu, Tanaka Yu-Ki, Suzuki Noriyuki, Ogra Yasumitsu

机构信息

Graduate School of Pharmaceutical Sciences, Chiba University, 1-8-1 Inohana, Chuo, Chiba, Chiba, 260-8675, Japan.

出版信息

Biochem Biophys Rep. 2022 Feb 1;29:101223. doi: 10.1016/j.bbrep.2022.101223. eCollection 2022 Mar.

DOI:10.1016/j.bbrep.2022.101223
PMID:35146136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8818919/
Abstract

Selenium is a chalcogen element that is essential in animals, but is highly toxic when ingested above the nutritional requirement. Selenite is used as a supplement in patients receiving total parenteral nutrition. However, the therapeutic and toxic doses of selenite are separated by a narrow range. This ambivalent character of selenite implies the presence of cellular mechanisms that precisely control selenite homeostasis. Here, we investigated mechanisms that determine cellular susceptibility to selenite exposure. The resistance to selenite exposure was significantly different among cell lines. We determined the expression levels of (thiopurine -methyltransferase) and (solute carrier family 4 member 1), which encode selenium methyltransferase and selenite transporter, respectively. We also examined the effect of inhibition of Band 3 protein activity, which is encoded by , on the cellular sensitivity to selenite. The data suggest that the expression level of is the determinant of cellular sensitivity to selenite.

摘要

硒是一种硫属元素,对动物至关重要,但当摄入量超过营养需求时具有高毒性。亚硒酸盐被用作接受全胃肠外营养患者的补充剂。然而,亚硒酸盐的治疗剂量和毒性剂量范围很窄。亚硒酸盐的这种矛盾特性意味着存在精确控制亚硒酸盐体内平衡的细胞机制。在此,我们研究了决定细胞对亚硒酸盐暴露易感性的机制。不同细胞系对亚硒酸盐暴露的抗性存在显著差异。我们测定了分别编码硒甲基转移酶和亚硒酸盐转运体的硫嘌呤甲基转移酶(TPMT)和溶质载体家族4成员1(SLC4A1)的表达水平。我们还研究了由SLC4A1编码的带3蛋白活性抑制对细胞对亚硒酸盐敏感性的影响。数据表明,TPMT的表达水平是细胞对亚硒酸盐敏感性的决定因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/4598e1d81ac4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/50777618775f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/c2b118791e5c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/f9a0ecd322df/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/4598e1d81ac4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/50777618775f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/c2b118791e5c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/f9a0ecd322df/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/180d/8818919/4598e1d81ac4/gr4.jpg

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HSe Induces Reductive Stress in HepG2 Cells and Activates Cell Autophagy by Regulating the Redox of HMGB1 Protein under Hypoxia.
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Theranostics. 2019 Feb 28;9(6):1794-1808. doi: 10.7150/thno.31841. eCollection 2019.
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