Saleh Khaled M M, Tarkhan Amneh H, Al-Zghoul Mohammad Borhan
Department of Applied Biological Sciences, Faculty of Science and Arts, Jordan University of Science and Technology, P.O. Box 3030, Irbid 22110, Jordan.
Department of Basic Medical Veterinary Sciences, Faculty of Veterinary Medicine, Jordan University of Science and Technology, P.O. Box 3030, Irbid 22110, Jordan.
Animals (Basel). 2020 Jan 13;10(1):126. doi: 10.3390/ani10010126.
Thermal stress is a major source of oxidative damage in the broiler chicken () due to the latter's impaired metabolic function. While heat stress has been extensively studied in broilers, the effects of cold stress on broiler physiologic and oxidative function are still relatively unknown. The present study aimed to understand how thermal manipulation (TM) might affect a broiler's oxidative response to post-hatch thermal stress in terms of the mRNA expression of the catalase, NADPH oxidase 4 (), and superoxide dismutase 2 () genes. During embryonic days 10 to 18, TM was carried out by raising the temperature to 39 °C at 65% relative humidity for 18 h/day. To induce heat stress, room temperature was raised from 21 to 35 °C during post-hatch days (PD) 28 to 35, while cold stress was induced during PD 32 to 37 by lowering the room temperature from 21 to 16 °C. At the end of the thermal stress periods, a number of chickens were euthanized to extract hepatic and splenic tissue from the heat-stressed group and cardiac, hepatic, muscular, and splenic tissue from the cold-stressed group. Catalase, , and expression in the heart, liver, and spleen were decreased in TM chickens compared to controls after both cold and heat stress. In contrast, the expression levels of these genes in the breast muscles of the TM group were increased or not affected. Moreover, TM chicks possessed an increased body weight (BW) and decreased cloacal temperature (T) compared to controls on PD 37. In addition, TM led to increased BW and lower T after both cold and heat stress. Conclusively, our findings suggest that TM has a significant effect on the oxidative function of thermally stressed broilers.
由于肉鸡代谢功能受损，热应激是其氧化损伤的主要来源。虽然热应激在肉鸡中已得到广泛研究，但冷应激对肉鸡生理和氧化功能的影响仍相对未知。本研究旨在了解热调控（TM）如何通过过氧化氢酶、NADPH氧化酶4（）和超氧化物歧化酶2（）基因的mRNA表达，影响肉鸡孵化后对热应激的氧化反应。在胚胎期第10至18天，通过将温度升至39°C、相对湿度65%、每天处理18小时来进行热调控。为诱导热应激，在孵化后天数（PD）28至35期间将室温从21°C升至35°C，而在PD 32至37期间通过将室温从21°C降至16°C来诱导冷应激。在热应激期结束时，对一些鸡实施安乐死，以从热应激组中提取肝脏和脾脏组织，从冷应激组中提取心脏、肝脏、肌肉和脾脏组织。与对照组相比，热调控鸡在冷应激和热应激后，心脏、肝脏和脾脏中的过氧化氢酶、和表达均降低。相比之下，热调控组胸肌中这些基因的表达水平升高或未受影响。此外，与PD 37时的对照组相比，热调控雏鸡体重增加，泄殖腔温度降低。此外，热调控导致冷应激和热应激后体重增加且温度降低。总之，我们的研究结果表明，热调控对热应激肉鸡的氧化功能有显著影响。
