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Am J Physiol Regul Integr Comp Physiol 297: R690-R698, 2009. First published June 24, 2009; doi:10.1152/ajpregu.90974.2008
0363-6119/09 $8.00
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ARTICLES

Olive oil-supplemented diet alleviates acute heat stress-induced mitochondrial ROS production in chicken skeletal muscle

Ahmad Mujahid, Yukio Akiba, and Masaaki Toyomizu

Nutritional Biochemistry of Animals, Graduate School of Agricultural Science, Tohoku University, Aoba-ku, Sendai, Japan

Submitted 2 December 2008 ; accepted in final form 17 June 2009

We have previously shown that avian uncoupling protein (avUCP) is downregulated on exposure to acute heat stress, stimulating mitochondrial reactive oxygen species (ROS) production and oxidative damage. In this study, we investigated whether upregulation of avUCP could attenuate oxidative damage caused by acute heat stress. Broiler chickens (Gallus gallus) were fed either a control diet or an olive oil-supplemented diet (6.7%), which has been shown to increase the expression of UCP3 in mammals, for 8 days and then exposed either to heat stress (34°C, 12 h) or kept at a thermoneutral temperature (25°C). Skeletal muscle mitochondrial ROS (measured as H2O2) production, avUCP expression, oxidative damage, mitochondrial membrane potential, and oxygen consumption were studied. We confirmed that heat stress increased mitochondrial ROS production and malondialdehyde levels and decreased the amount of avUCP. As expected, feeding birds an olive oil-supplemented diet increased the expression of avUCP in skeletal muscle mitochondria and decreased ROS production and oxidative damage. Studies on mitochondrial function showed that heat stress increased membrane potential in state 4, which was reversed by feeding birds an olive oil-supplemented diet, although no differences in basal proton leak were observed between control and heat-stressed groups. These results show that under heat stress, mitochondrial ROS production and olive oil-induced reduction of ROS production may occur due to changes in respiratory chain activity as well as avUCP expression in skeletal muscle mitochondria.

mitochondria; reactive oxygen species; membrane potential; uncoupling protein; proton leak



Address for reprint requests and other correspondence: M. Toyomizu, Nutritional Biochemistry of Animals, Life Sciences, Graduate School of Agricultural Science, Tohoku Univ., 1-1 Tsutsumidori-Amamiyamachi, Aoba-ku, Sendai 981-8555, Japan (e-mail: toyomizu{at}bios.tohoku.ac.jp)







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