State Key Laboratory of Animal Nutrition, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing 100193, P. R. China.
Poult Sci. 2010 Jan;89(1):115-22. doi: 10.3382/ps.2009-00318.
This study investigated the effects of different acute high ambient temperatures on dysfunction of hepatic mitochondrial respiration, the antioxidative enzyme system, and oxidative injury in broiler chickens. One hundred twenty-eight 6-wk-old broiler chickens were assigned randomly to 4 groups and subsequently exposed to 25 (control), 32, 35, and 38 degrees C (RH, 70 +/- 5%) for 3 h, respectively. The rectal temperatures, activity of antioxidative enzymes (superoxide dismutase, catalase, and glutathione peroxidase), content of malondialdehyde and protein carbonyl, and the activity of mitochondrial respiratory enzymes were determined. The results showed that exposure to high ambient temperature induced a significant elevation of rectal temperature, antioxidative enzyme activity, and formation of malondialdehyde and protein carbonyl, as well as dysfunction of the mitochondrial respiratory chain in comparison with control (P < 0.05). Almost all of the indicators changed in a temperature-dependent manner with the gradual increase of ambient temperature from 32 to 38 degrees C; differences in each parameter (except catalase) among the groups exposed to different high ambient temperatures were also statistically significant (P < 0.05). The results of the present study suggest that, in the broiler chicken model used here, acute exposure to high temperatures may depress the activity of the mitochondrial respiratory chain. This inactivation results subsequently in overproduction of reactive oxygen species, which ultimately results in oxidative injury. However, this hypothesis needs to be evaluated more rigorously in future studies. It has also been shown that, with the gradual increase in temperature, the oxidative injury induced by heat stress in broiler chickens becomes increasingly severe, and this stress response presents in a temperature-dependent manner in the temperature range of 32 to 38 degrees C.
本研究探讨了不同急性高环境温度对肉鸡肝线粒体呼吸功能障碍、抗氧化酶系统和氧化损伤的影响。将 128 只 6 周龄的肉鸡随机分为 4 组，分别暴露于 25（对照）、32、35 和 38°C（相对湿度，70 ± 5%）3 h。测定直肠温度、抗氧化酶（超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶）活性、丙二醛和蛋白质羰基含量以及线粒体呼吸酶活性。结果表明，与对照组相比，高温暴露导致直肠温度、抗氧化酶活性、丙二醛和蛋白质羰基的形成以及线粒体呼吸链功能障碍显著升高（P < 0.05）。从 32°C 到 38°C，随着环境温度的逐渐升高，几乎所有指标都呈温度依赖性变化；暴露于不同高温环境的各组之间的每个参数（除过氧化氢酶外）差异均有统计学意义（P < 0.05）。本研究结果表明，在本研究中使用的肉鸡模型中，急性暴露于高温可能会抑制线粒体呼吸链的活性。这种失活随后导致活性氧的过度产生，最终导致氧化损伤。然而，这一假设需要在未来的研究中更严格地评估。研究还表明，随着温度的逐渐升高，肉鸡因热应激引起的氧化损伤变得越来越严重，这种应激反应在 32 至 38°C 的温度范围内呈温度依赖性。
