The role of necroptosis and apoptosis through the oxidative stress pathway in the liver of selenium-deficient swine

文献类型： 外文期刊

第一作者： Zhang, Yuan

作者： Zhang, Yuan;Yu, Dahai;Tang, Chaohua;Zhang, Yuan;Yu, Dahai;Zhang, Jiuli;Zhang, Ziwei;Bao, Jun;Zhang, Ziwei

作者机构：

期刊名称：METALLOMICS （ 影响因子：4.526； 五年影响因子：4.69 ）

ISSN： 1756-5901

年卷期： 2020 年 12 卷 4 期

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收录情况： SCI

摘要： Necroptosis is regarded as a new paradigm of cell death that plays a key role in the liver damage observed with selenium (Se) deficiency. Se deficiency has a significant impact on the livestock and poultry industries. Previous studies have confirmed that Se deficiency causes serious injury to the swine liver; however, it is unclear whether this liver damage is the result of necroptosis and apoptosis. To understand the damage induced by Se deficiency, swine were divided into a control group and Se-deficient group. The results showed that in the liver of swine, Se deficiency initiated apoptosis by increasing the expression of cysteinyl aspartate specific proteinase 3 (caspase-3), cysteinyl aspartate specific proteinase 9 (caspase-9) and BCL-2 antagonist/killer (BAK) at both the mRNA and protein levels and by decreasing the B cell lymphoma/leukemia 2 (BCL-2) levels compared with the levels in the control group. Meanwhile, compared with the control group, necroptosis was confirmed in the liver of Se-deficient swine through increased the expression of mixed lineage kinase domain like pseudokinase (MLKL) and receptor interacting serine/threonine kinase 1 (RIPK1) at both the mRNA and protein levels. In addition, the activities of catalase (CAT), nitric oxide (NO), and total antioxidative capacity (T-AOC) were clearly increased (P< 0.05), and the activities of OH- and total nitric oxide synthase (TNOS) were obviously decreased (P< 0.05), whereas in the Se-deficient group, the hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels were obviously increased (P< 0.05) compared with those in the control group. Moreover, the number of apoptotic cells was increased significantly in the Se-deficient group, and the liver tissues showed obvious necroptosis damage. These results show that Se deficiency induces apoptosis and necroptosis through the oxidative stress pathway in the swine liver.

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