This study aimed to investigate the effects of different acute high ambient temperatures on redox status in liver of broilers. A total of 144 35-day-old Arbor Acres broilers were randomly divided into 4 groups with 6 replicates of 6 birds each and subsequently distributed in different environment chambers for acute heat stress. The temperature of 4 environment chambers were set to 26°C (control), 29°C, 32°C, 35°C for 6 h, respectively. Various indicators were tested to evaluate hepatic redox status. Then, the hallmarks of hepatocellular antioxidant and apoptosis were measured by qRT-PCR and Western Blot. The results showed that with the ambient temperature increase (i) the content of hydrogen peroxide (H2O2) and protein carbonyl (PC) in the liver of broilers increased significantly (P < 0.05), but the content of malondialdehyde (MDA) and 8-hydroxyguanosine (8-OHdG) was not affected; (ii) the activity of catalase (CAT) and glutathione reductase (GR) increased significantly (P < 0.05). Similarly, the superoxide dismutase (SOD) had an increasing tendency (P = 0.07), and the content of the reduced glutathione (GSH) was also significantly increased (P < 0.05) under high temperature; (iii) the heat shock protein (HSP70), nuclear factor erythroid-2-related factor 2 (Nrf2), and other antioxidant gene (HO-1, NQO1, GCLc, GST, SOD1, SOD2, CAT, Prx3) were upregulated in broilers liver. Moreover, the protein level of HSP70, Nrf2, and Prx3 were also upregulated; (iv) high temperature upregulated the antiapoptotic gene expression (BCL-2); however, the proapoptotic genes (BAK1, caspase-3, and caspase-9) did not change significantly; meanwhile, there was no significant changes in the protein level of caspase-3 and caspase-9. The results of this study indicated that 35-day-old Arbor Acres broilers have a certain tolerance to oxidative stress induced by high ambient temperature. Six hours of acute heat stress-activated Nrf2 signaling pathway. Meanwhile, the expression of related antioxidant genes and proteins is upregulated, consequently resulted in increased antioxidant enzymes activity and GSH. These effects enable the body to scavenge large amounts of reactive oxygen species produced by high temperature and prevent the occurrence of apoptosis.

中文翻译：

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不同环境温度急性热应激对肉鸡肝脏氧化还原状态的影响

本研究旨在探讨不同急性高温环境对肉鸡肝脏氧化还原状态的影响。将 144 只 35 日龄 Arbor Acres 肉鸡随机分为 4 组，每组 6 个重复，每组 6 只鸡，随后分布在不同的环境室中进行急性热应激。4个环境室的温度分别设置为26℃（对照）、29℃、32℃、35℃，持续6小时。测试各种指标来评估肝脏氧化还原状态。然后，通过 qRT-PCR 和 Western Blot 测量肝细胞抗氧化和凋亡的标志。结果表明，随着环境温度的升高（i），肉鸡肝脏中过氧化氢（H2O2）和蛋白质羰基（PC）的含量显着增加（P < 0.05），但丙二醛（MDA）和8-羟基鸟苷（8-OHdG）不受影响；(ii)过氧化氢酶(CAT)和谷胱甘肽还原酶(GR)的活性显着增加(P < 0.05)。同样，高温下超氧化物歧化酶（SOD）有增加趋势（P = 0.07），还原型谷胱甘肽（GSH）含量也显着增加（P < 0.05）；(iii) 热休克蛋白（HSP70）、核因子红细胞2相关因子2（Nrf2）和其他抗氧化基因（HO-1、NQO1、GCLc、GST、SOD1、SOD2、CAT、Prx3）在肉鸡肝脏。此外，HSP70、Nrf2和Prx3的蛋白水平也上调；(iv)高温上调抗凋亡基因表达(BCL-2)；然而，促凋亡基因（BAK1、caspase-3和caspase-9）没有显着变化；同时，caspase-3和caspase-9的蛋白水平没有明显变化。本研究结果表明，35日龄Arbor Acres肉鸡对高环境温度诱导的氧化应激具有一定的耐受性。六个小时的急性热应激激活 Nrf2 信号通路。同时，相关抗氧化基因和蛋白质的表达上调，从而导致抗氧化酶活性和GSH增加。这些作用使机体能够清除高温产生的大量活性氧，防止细胞凋亡的发生。