The role of necroptosis and apoptosis through the oxidative stress pathway in the liver of selenium-deficient swine. Issue 4 (16th March 2020)

• Record Type: Journal Article
• Authors: Zhang, Yuan; Yu, Dahai; Zhang, Jiuli; Bao, Jun; Tang, Chaohua; Zhang, Ziwei
• Is Part Of: Metallomics. Volume 12:Issue 4(2020)
• Page Start: 607
• Page End: 616
• Publication Date: 2020-03-16
• Subjects: Metals -- Physiological effect -- Periodicals; 572.51
• DOI: 10.1039/c9mt00295b
• Languages: English
• ISSNs: 1756-5901

Abstract

Abstract : Necroptosis is regarded as a new paradigm of cell death that plays a key role in the liver damage observed with selenium (Se) deficiency. Abstract : 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 (H2 O2 ) 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.