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高温诱导的氧化应激通过调节肝脏和空肠中的锌转运体和金属硫蛋白影响肉鸡的全身锌稳态。

High Temperature-Induced Oxidative Stress Affects Systemic Zinc Homeostasis in Broilers by Regulating Zinc Transporters and Metallothionein in the Liver and Jejunum.

机构信息

Department of Animal Science, Shandong Agricultural University, Taian, Shandong 271018, China.

Precision Livestock and Nutrition Unit, Gembloux Agro-Bio Tech, University of Liège, Gembloux 5030, Belgium.

出版信息

Oxid Med Cell Longev. 2022 Mar 28;2022:1427335. doi: 10.1155/2022/1427335. eCollection 2022.

DOI:10.1155/2022/1427335
PMID:35387265
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8979716/
Abstract

To investigate the change in zinc homeostasis of broilers under heat stress, 512 broiler chickens were raised to the age of 28 days. The broilers were then assigned to heat stress and normal temperature (36.0°C vs. 26.0°C) groups for 7 days. The results showed that oxidative stress induced by high temperature had a negative effect on the growth performance of broilers. Heat stress altered zinc homeostasis and led to a redistribution of zinc in broilers, which was reflected in increased zinc concentrations in the jejunum, liver, and tibia. Upregulation of the expression of the zinc exporter and importers and in the jejunum indicated that more zinc was absorbed and transported from the jejunum into the blood, while the liver increased its capacity to hold zinc through upregulation of metallothionein () expression, which was achieved by reducing expression and upregulating the expression of the importer . The pathway was mediated by zinc transporters, but the capacity of to chelate and release zinc ions also played a crucial role. The mechanism of alterations in zinc homeostasis under heat stress was revealed by the changes in zinc transporters and levels in the intestine and liver. Heat stress also altered cecal microbial diversity and reduced the relative abundances of and . In conclusion, broilers altered systemic zinc homeostasis through the regulation of zinc transporters and in the liver and jejunum to resist oxidative stress induced by high temperature.

摘要

为了研究热应激对肉鸡锌稳态的影响,选择 512 只肉鸡饲养至 28 日龄。然后,将肉鸡分为热应激和常温(36.0°C 对 26.0°C)组,持续 7 天。结果表明,高温引起的氧化应激对肉鸡的生长性能产生负面影响。热应激改变了锌稳态,导致肉鸡体内锌重新分布,表现为空肠、肝脏和胫骨中的锌浓度增加。空肠中锌输出蛋白 和 以及锌输入蛋白 表达上调表明,更多的锌从空肠吸收并转运到血液中,而肝脏通过降低 表达和上调锌输入蛋白 的表达来增加其对锌的保持能力 。该途径由锌转运蛋白介导,但 螯合和释放锌离子的能力也起着关键作用。肠道和肝脏中锌转运蛋白和 水平的变化揭示了热应激下锌稳态改变的机制。热应激还改变了盲肠微生物多样性,降低了 和 的相对丰度。总之,肉鸡通过调节肝脏和空肠中的锌转运蛋白和 来改变全身锌稳态,以抵抗高温引起的氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/2cdfcf89e8b2/OMCL2022-1427335.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/a15fad02dc7e/OMCL2022-1427335.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/afa67152a5fe/OMCL2022-1427335.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/57c32bd2a1e3/OMCL2022-1427335.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/19220807a870/OMCL2022-1427335.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/4fff09183377/OMCL2022-1427335.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/3c11d58e18b4/OMCL2022-1427335.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/2cdfcf89e8b2/OMCL2022-1427335.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/a15fad02dc7e/OMCL2022-1427335.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/afa67152a5fe/OMCL2022-1427335.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/57c32bd2a1e3/OMCL2022-1427335.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/19220807a870/OMCL2022-1427335.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/4fff09183377/OMCL2022-1427335.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/3c11d58e18b4/OMCL2022-1427335.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4921/8979716/2cdfcf89e8b2/OMCL2022-1427335.007.jpg

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