scholarly journals Different Sources of Copper Effect on Intestinal Epithelial Cell: Toxicity, Oxidative Stress, and Metabolism

Metabolites ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 11
Author(s):  
Runxian Li ◽  
Yang Wen ◽  
Gang Lin ◽  
Chengzhen Meng ◽  
Pingli He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Epithelial Cell ◽  
Protein Expression ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Intestinal Epithelial ◽  
Protein Expression Level ◽  
Treatment Groups ◽  
All Treatment

Copper (Cu) is widely used in the swine industry to improve the growth performance of pigs. However, high doses of copper will induce cell damage and toxicity. The aim of this study was to evaluate toxicity, bioavailability, and effects on metabolic processes of varying copper sources using porcine intestinal epithelial cells (IPEC-J2) as a model. The IPEC-J2 were treated with two doses (30 and 120 μM) of CuSO4, Cu Glycine (Cu-Gly), and Cu proteinate (Cu-Pro) for 10 h, respectively. Cell damage and cellular copper metabolism were measured by the changes in cell viability, copper uptake, oxidative stress biomarkers, and gene/protein expression levels. The results showed that cell viability and ratio of reduced and oxidized glutathione (GSH/GSSG) decreased significantly in all treatment groups; intracellular copper content increased significantly in all treatment groups; total superoxide dismutase (SOD) activity increased significantly in the 120 μM exposed groups; SOD1 protein expression levels were significantly upregulated in 30 μM Cu-Pro, 120 μM Cu-Gly, and 120 μM Cu-Pro treatment groups; intracellular reactive oxygen species (ROS) generation and malondialdehyde (MDA) content increased significantly in 30 μM treatment groups and 120 μM CuSO4 treatment group. CTR1 and ATP7A gene expression were significantly downregulated in the 120 μM exposed groups. While upregulation of ATOX1 expression was observed in the presence of 120 μM Cu-Gly and Cu-Pro. ASCT2 gene expression was significantly upregulated after 120 μM Cu-Glycine and CuSO4 exposure, and PepT1 gene expression was significantly upregulated after Cu-Pro exposure. In addition, CTR1 protein expression level decreased after 120 μM CuSO4 and Cu-Gly exposure. PepT1 protein expression level was only upregulated after 120 μM Cu-Pro exposure. These findings indicated that extra copper supplementation can induce intestinal epithelial cell injury, and different forms of copper may have differing effects on cell metabolism.

1H-NMR Based Metabolomics Study of the Intestinal Epithelial Cell (IEC-6) Under the Oxidative Stress

2010 ◽  
Vol 158 (2) ◽  
pp. 256 ◽  
Author(s):  
K. Nakata ◽  
N. Sato ◽  
T. Asakura ◽  
K. Hirakawa ◽  
R. Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
1H Nmr ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Metabolomics Study

scholarly journals Total Intermittent Pringle Maneuver during Liver Resection Can Induce Intestinal Epithelial Cell Damage and Endotoxemia

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30539 ◽  
Author(s):  
Simon A. W. G. Dello ◽  
Kostan W. Reisinger ◽  
Ronald M. van Dam ◽  
Marc H. A. Bemelmans ◽  
Toin H. van Kuppevelt ◽  
...  
Keyword(s):  
Liver Resection ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Cell Damage ◽  
Pringle Maneuver ◽  
Intestinal Epithelial

Regulation of α1-antitrypsin gene expression in human intestinal epithelial cell line Caco-2 by HNF-1α and HNF-4

1999 ◽  
Vol 276 (5) ◽  
pp. G1181-G1194 ◽  
Author(s):  
Chaobin Hu ◽  
David H. Perlmutter
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Epithelial Cell Line ◽  
Mrna Levels ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cell ◽  
Mobility Shift ◽  
Electrophoretic Mobility Shift Assays ◽  
Enterocyte Differentiation

There is still relatively limited information about mechanisms of gene expression in enterocytes and mechanisms by which gene expression is regulated during enterocyte differentiation. Using the human intestinal epithelial cell line Caco-2, which spontaneously differentiates from a cryptlike to a villouslike enterocyte, we have previously shown that there is a marked increase in transcription of the well-characterized α1-antitrypsin (α1-AT) gene during enterocyte differentiation. In this study we examined the possibility of identifying the cis-acting elements and trans-acting DNA-binding proteins responsible for expression of the α1-AT gene in Caco-2 cells during differentiation. Footprint analysis and electrophoretic mobility shift assays showed that hepatocyte nuclear factor-1α (HNF-1α), HNF-1β, and HNF-4 from nuclear extracts of Caco-2 cells specifically bound to two regions in the proximal promoter of the α1-AT gene. Cotransfection studies showed that HNF-1α and HNF-4 had a synergistic effect on α1-AT gene expression. RNA blot analysis showed that HNF-1α and HNF-4 mRNA levels and electrophoretic mobility shift assays showed that HNF-1α binding activity increase coordinately with α1-AT mRNA levels during differentiation of Caco-2 cells. Finally, overexpression of antisense ribozymes for HNF-1α in Caco-2 cells resulted in a selective decrease in endogenous α1-AT gene expression. Together, these results provide evidence that HNF-1α and HNF-4 play a role in the mechanism by which the α1-AT gene is upregulated during enterocyte differentiation in the model Caco-2 cell system.

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