Alterations of the extracellular matrix of lung during zinc deficiency

Suboptimal intake of Zn is one of the most common nutritional problems worldwide. Previously, we have shown that Zn deficiency (ZD) produces oxidative and nitrosative stress in the lung of rats. We analyse the effect of moderate ZD on the expression of several intermediate filaments of the cytoskeleton, as well as the effect of restoring Zn during the refeeding period. Adult male rats were divided into three groups: Zn-adequate control (CO) group; ZD group; Zn-refeeding group. CerbB-2 and proliferating cell nuclear antigen (PCNA) expression was increased in the ZD group while the other parameters did not change. During the refeeding time, CerbB-2, cytokeratins, vimentin and PCNA immunostaining was higher than that in the CO group. The present findings indicate that the overexpression of some markers could lead to the fibrotic process in the lung. Perhaps ZD implications must be taken into account in health interventions because an inflammation environment is associated with ZD in the lung.

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Quercetin Modulates Aging Induced-Testicular Damage Via Increasing the Antioxidant Defense and the Immunolocalization of the Proliferating Cell Nuclear Antigen in Male Rats

Pakistan Journal of Zoology ◽

10.17582/journal.pjz/20191012181016 ◽

2020 ◽

Author(s):

Eman A. Al-Shahari

Keyword(s):

Proliferating Cell Nuclear Antigen ◽

Antioxidant Defense ◽

Male Rats ◽

Nuclear Antigen ◽

Testicular Damage ◽

Proliferating Cell

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C/EBPδ protects from radiation-induced intestinal injury and sepsis by suppression of inflammatory and nitrosative stress

Scientific Reports ◽

10.1038/s41598-019-49437-x ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 2

Author(s):

Sudip Banerjee ◽

Qiang Fu ◽

Sumit K. Shah ◽

Stepan B Melnyk ◽

Esta Sterneck ◽

...

Keyword(s):

Nitrosative Stress ◽

Intestinal Barrier ◽

Intestinal Injury ◽

Nuclear Antigen ◽

Intestinal Damage ◽

Oxidative And Nitrosative Stress ◽

Tnf Α ◽

Radiation Induced ◽

Villous Height ◽

Proliferating Cell

Abstract Ionizing radiation (IR)-induced intestinal damage is characterized by a loss of intestinal crypt cells, intestinal barrier disruption and translocation of intestinal microflora resulting in sepsis-mediated lethality. We have shown that mice lacking C/EBPδ display IR-induced intestinal and hematopoietic injury and lethality. The purpose of this study was to investigate whether increased IR-induced inflammatory, oxidative and nitrosative stress promote intestinal injury and sepsis-mediated lethality in Cebpd−/− mice. We found that irradiated Cebpd−/− mice show decreased villous height, crypt depth, crypt to villi ratio and expression of the proliferation marker, proliferating cell nuclear antigen, indicative of intestinal injury. Cebpd−/− mice show increased expression of the pro-inflammatory cytokines (Il-6, Tnf-α) and chemokines (Cxcl1, Mcp-1, Mif-1α) and Nos2 in the intestinal tissues compared to Cebpd+/+ mice after exposure to TBI. Cebpd−/− mice show decreased GSH/GSSG ratio, increased S-nitrosoglutathione and 3-nitrotyrosine in the intestine indicative of basal oxidative and nitrosative stress, which was exacerbated by IR. Irradiated Cebpd-deficient mice showed upregulation of Claudin-2 that correlated with increased intestinal permeability, presence of plasma endotoxin and bacterial translocation to the liver. Overall these results uncover a novel role for C/EBPδ in protection against IR-induced intestinal injury by suppressing inflammation and nitrosative stress and underlying sepsis-induced lethality.

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