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      Effects of cage and floor rearing system on the factors of antioxidant defense and inflammatory injury in laying ducks

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          Abstract

          Background

          Cage-rearing in laying ducks, as a novel rearing system, not only fundamentally solves the pollution problem of the duck industry and improve bio-safety and product quality but also exhibits more benefits by implementing standardized production compared with the floor-rearing. Of course, this system also brings some welfare problems and stress injuries to layers due to lack of water environment and limited activities in the cages. However, the effects on the factors of antioxidant defense and inflammatory injury in the early cage stage are not well-understood.

          Results

          In this study, eighty Shaoxing layers were reared on floor and in cages from 12 weeks of age. The ducks were caged 1, 2, 4, 7, and 10 days, the factors of antioxidant defense and inflammatory injury were investigated. The results showed that the caged ducks suffered liver injury to a certain extent when the ducks were just put into the cages. Analysis of antioxidant enzyme activities indicated that the different rearing system could not affect the change of antioxidant capacities, while the liver malondialdehyde (MDA) level was significant higher in the 2-d, 7-d, and 10-d ducks compared with the 1-d ducks during the change of days, while catalase (CAT) activity showed the opposite results. Additionally, quantitative real-time PCR (qRT-RCR) revealed that the relative mRNA levels of endoplasmic reticulum (ER) stress-related gene (CHOP and GRP78) were significantly upregulated in cage rearing ducks compared to that of the floor rearing ducks. Moreover, the mRNA levels of inflammatory cytokines including cycloxygenase-2 (COX-2), nitric oxide synthase (iNOS), Interleukin 1 beta (IL-1β), Interleukin 2 (IL-2) and Interleukin 6 (IL-6), were also increased significantly in caged layers.

          Conclusions

          Taken together, although antioxidant defense has no obvious effect on cage stress, the stress levels of laying ducks vary greatly in the early cage stage, which not only caused liver tissue damage to some extent, but also resulted in increases in the expression of the factors of inflammatory injury. Therefore, we recommend that anti-stress agents should be added in the feed to alleviate the stress in the early cage stage.

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          Most cited references19

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          Biomarkers of oxidative stress study II: are oxidation products of lipids, proteins, and DNA markers of CCl4 poisoning?

          Oxidation products of lipids, proteins, and DNA in the blood, plasma, and urine of rats were measured as part of a comprehensive, multilaboratory validation study searching for noninvasive biomarkers of oxidative stress. This article is the second report of the nationwide Biomarkers of Oxidative Stress Study using acute CCl4 poisoning as a rodent model for oxidative stress. The time-dependent (2, 7, and 16 h) and dose-dependent (120 and 1200 mg/kg i.p.) effects of CCl4 on concentrations of lipid hydroperoxides, TBARS, malondialdehyde (MDA), isoprostanes, protein carbonyls, methionine sulfoxidation, tyrosine products, 8-hydroxy-2'-deoxyguanosine (8-OHdG), leukocyte DNA-MDA adducts, and DNA-strand breaks were investigated to determine whether the oxidative effects of CCl4 would result in increased generation of these oxidation products. Plasma concentrations of MDA and isoprostanes (both measured by GC-MS) and urinary concentrations of isoprostanes (measured with an immunoassay or LC/MS/MS) were increased in both low-dose and high-dose CCl4-treated rats at more than one time point. The other urinary markers (MDA and 8-OHdG) showed significant elevations with treatment under three of the four conditions tested. It is concluded that measurements of MDA and isoprostanes in plasma and urine as well as 8-OHdG in urine are potential candidates for general biomarkers of oxidative stress. All other products were not changed by CCl4 or showed fewer significant effects.
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            Unfolded proteins and endoplasmic reticulum stress in neurodegenerative disorders

            Abstract The stimuli for neuronal cell death in neurodegenerative disorders are multi-factorial and may include genetic predisposition, environmental factors, cellular stressors such as oxidative stress and free radical production, bioenergy failure, glutamate-induced excitotoxicity, neuroinflammation, disruption of Ca2+-regulating systems, mitochondrial dysfunction and misfolded protein accumulation. Cellular stress disrupts functioning of the endoplasmic reticulum (ER), a critical organelle for protein quality control, leading to induction of the unfolded protein response (UPR). ER stress may contribute to neurodegeneration in a range of neurodegenerative disorders. This review summarizes the molecular events occurring during ER stress and the unfolded protein response and it specifically evaluates the evidence suggesting the ER stress response plays a role in neurodegenerative disorders.
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              Metabolic characteristics and oxidative damage to skeletal muscle in broiler chickens exposed to chronic heat stress.

              Emerging evidence has shown that acute heat exposure affects metabolic characteristics and causes oxidative damage to skeletal muscle in birds. Little is known, however, about such phenomena under chronic heat stress conditions. To address this, we designed the present study to determine the influence of cyclic (32 to 24 to 32 degrees C: 32 degrees C for 8 h/d, 32-24-32HS ), and constant (32 and 34 degrees C, 32HS and 34HS, respectively) heat exposure on the metabolic and peroxide status in skeletal muscle of 4-wk-old male broiler chickens. Heat stress, particularly in the 32HS and 34HS groups, depressed feed intake and growth, while cyclic high temperature gave rise to a less severe stress response in performance terms. Malondialdehyde (MDA) levels in skeletal muscle were enhanced (P<0.05) by constant heat treatment; the degree of enhancement was not as large as the changes observed in our previous 'acute' heat stress model. The 3HADH (3-hydroxyacyl CoA dehydrogenase related to fatty acid oxidation) and CS (citrate synthase) enzyme activities were lowered (P<0.05) by both the cyclic and constant 34HS treatments, and constant 34HS group, respectively. These results suggest that chronic heat exposure decreases metabolic oxidation capacity in skeletal muscle of broiler chickens. On exposure to chronic heat stress, GPx activity remained relatively constant, though a temperature-dependent elevation in Cu/Zn-SOD activity was observed, implying that anti-oxidation ability was disturbed by the chronic stress condition. From these results it can be concluded that chronic heat stress did not induce oxidative damage to a major extent. This may probably be due to a decrease in metabolic oxidation capacity or due to a self-propagating scavenging system, though the system was not fully activated. Copyright 2009 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                zyang@yzu.edu.cn
                gtt19931029@126.com
                1015080153@qq.com
                kuaileqianjin@163.com
                ligq@mail.zaas.ac.cn
                glyzzj2017@163.com
                guiliu08@163.com
                xswu@yzu.edu.cn
                zengtao4009@126.com
                xuqi@yzu.edu.cn
                ghchen@yzu.edu.cn
                lulizhibox@163.com
                Journal
                BMC Genet
                BMC Genet
                BMC Genetics
                BioMed Central (London )
                1471-2156
                30 December 2019
                30 December 2019
                2019
                : 20
                : 103
                Affiliations
                [1 ]GRID grid.268415.c, Jiangsu Key Laboratory for Animal Genetic, Breeding and Molecular Design, , Yangzhou University, ; Yangzhou, 225009 Jiangsu China
                [2 ]ISNI 0000 0000 9883 3553, GRID grid.410744.2, Institute of Animal Husbandry and Veterinary Medicine, Zhejiang Academy of Agricultural Sciences, ; Zhejiang, 310021 Hangzhou China
                [3 ]Key Laboratory of Information Traceability for Agricultural Products, Ministry of Agriculture of China, Hangzhou, 310021 Zhejiang China
                [4 ]Guiliu Animal Husbandry Company, Zhoukou, 450000 Henan China
                [5 ]GRID grid.268415.c, Key Laboratory of Animal Genetics, Breeding and Molecular Design of Jiangsu Province, , Yangzhou University, ; Yangzhou, 225009 PR China
                Author information
                http://orcid.org/0000-0002-2413-5589
                Article
                806
                10.1186/s12863-019-0806-0
                6937681
                31888457
                02d78898-e68d-4b05-8e1f-69c915ece0fe
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 27 December 2018
                : 22 December 2019
                Funding
                Funded by: National Natural Science Foundation of China (CN)
                Award ID: 31402066
                Funded by: the National Key Research and Development Project
                Award ID: 2018YFD0501504
                Funded by: the Research Program of Zhejiang Basic Public Welfare
                Award ID: LGN18C170003
                Funded by: the Natural Science Foundation of Zhejiang Province
                Award ID: LQ17C170003
                Funded by: the Natural Science Foundation of China
                Award ID: 31702106
                Award ID: 31572385
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2019

                Genetics
                cage rearing,duck,antioxidant enzymes,inflammatory cytokines
                Genetics
                cage rearing, duck, antioxidant enzymes, inflammatory cytokines

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