Time course of ROS production in skeletal muscle mitochondria from chronic heat-exposed broiler chicken

被引：74

作者：

Azad, M. A. K. ^{[1
]}

Kikusato, M. ^{[1
]}

Sudo, S. ^{[1
]}

Amo, T. ^{[2
]}

Toyomizu, M. ^{[1
]}

机构：

[1] Tohoku Univ, Grad Sch Agr Sci, Aoba Ku, Sendai, Miyagi 9818555, Japan

[2] Natl Def Acad, Dept Appl Chem, Yokosuka, Kanagawa 2398686, Japan

来源：

COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR & INTEGRATIVE PHYSIOLOGY | 2010年 / 157卷 / 03期

关键词：

Mitochondria; ROS; Oxygen consumption; Membrane potential; Chronic heat stress; RAT-LIVER MITOCHONDRIA; OXIDATIVE-PHOSPHORYLATION; PROTON LEAK; SUPEROXIDE; RESPIRATION; STRESS;

D O I：

10.1016/j.cbpa.2010.07.011

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

This study was designed to elucidate physiological changes of skeletal muscle mitochondria from broiler chickens (Gallus gallus) during chronic heat exposure. Chickens (19-day-old) were exposed to either constant heat stress (34 degrees C) or kept at control temperature (24 degrees C) for 14 days. Mitochondrial ROS production for control group showed little changes during the experimental periods, whereas that for the heat-stressed group was increased after 3, 5 and 9 days of heat exposure and returned to original levels at day 14. Mitochondrial membrane potential in state 4 for heat-stressed birds was higher than those of control birds after 3 and 5 days, but was not at day 14. Mitochondrial oxygen consumption rate in state 3 was increased after 3 and 5 days, and also returned to original levels by day 14. These results suggest that chronic heat stress induces increased ROS production in skeletal muscle mitochondria, probably via elevation of the membrane potential in state 4, resulting from enhanced oxygen consumption in the initial stage of heat exposure. These physiological changes were no longer observed at day 14, possibly because the animals had acclimatized to environmental heat stress. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：266 / 271

页数：6

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