Effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration, ROS production and lipid peroxidation in broiler chickens

• Published in: Comparative biochemistry and physiology. Toxicology & pharmacology Vol. 151; no. 2; pp. 204 - 208
• Main Authors: Yang, Lin, Tan, Gao-Yi, Fu, Yu-Qiang, Feng, Jin-Hai, Zhang, Min-Hong
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.03.2010
• Subjects: Acute heat stress; Analysis of Variance; Animals; Broiler chicken; Catalase - metabolism; Cell Respiration - physiology; Chickens - metabolism; Glutathione Peroxidase - metabolism; Hot Temperature; Lipid peroxidation; Lipid Peroxidation - physiology; Male; Mitochondria, Liver - metabolism; Mitochondrial respiratory complex; Reactive oxygen species; Reactive Oxygen Species - metabolism; Stress, Physiological - physiology; Superoxide Dismutase - metabolism; Time Factors; Lipid peroxidation; Mitochondrial respiratory complex; Broiler chicken; Reactive oxygen species; Acute heat stress
• ISSN: 1532-0456; 1878-1659
• DOI: 10.1016/j.cbpc.2009.10.010

In order to investigate the effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration, production of reactive oxygen species (ROS) and lipid peroxidation in broiler chickens, 128 six-week-old broiler chickens were kept in a controlled-environment chamber. The broiler chickens were initially kept at 25 °C (relative humidity, RH, 70 ± 5%) for 6 d and subsequently exposed to 35 °C (RH, 70 ± 5%) for 3 h, then the heat stress was removed and the temperature returned to 25 °C (RH, 70 ± 5%). Blood and liver samples were obtained before heat exposure and at 0 (at the end of the three-hour heating episode, this group is also abbreviated as the HT group), 1, 2, 4, 8, 12 h after the stress was removed. The results showed that acute heat stress induced a significant production of ROS, function of the mitochondrial respiratory chain, antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activity, and formation of malondialdehybe (MDA). Within the first 12 h after removal of the heat stress, the acute modification of the above parameters induced by heat stress gradually approached to pre-heat levels. The results of the present study suggest that acute exposure to high temperatures may depress the activity of the mitochondrial respiratory chain. This leads to over-production of ROS, which ultimately results in lipid peroxidation and oxidative stress. When the high temperature was removed, the production of ROS, mitochondrial respiratory function and oxidative injury that were induced by acute heat exposure gradually approached the levels observed before heating, in a time-dependent manner.