期刊
FEBS LETTERS
卷 581, 期 18, 页码 3461-3467出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2007.06.051
关键词
adenine nucleotide translocator; carnitine palmitoyl transferase; fatty acid oxidation enzyme; heat stress; reactive oxygen species; uncoupling protein
资金
- NIDDK NIH HHS [DK 52581] Funding Source: Medline
We have shown that heat-stressed birds exhibit increased superoxide production in skeletal muscle mitochondria. To determine the precise mechanism for this effect, here we studied not only progressive, but also sequential changes in superoxide production, anion carriers and substrate oxidation in mitochondria of heat-stressed chickens. Exposure to acute heat stress (34 degrees C for 6, 12 and 18 h) stimulated pectoralis muscle mitochondrial superoxide production. Heat stress-induced downregulations of avUCP gene transcripts and mitochondrial avUCP protein content were time-dependent: avUCP gene transcript was decreased after 6 h, while avUCP protein content was only downregulated after 12 h of heat stress. Avian adenine nucleotide translocator (avANT) gene transcripts were not changed on exposure to heat stress, suggesting that avANT may not be involved in the regulation of superoxide production in the muscle mitochondria of heat-stressed chickens. During the initial stage of acute heat stress beta-oxidation enzymes gene transcripts and activity were upregulated, with elevated plasma non-esteritied fatty acid levels and increased expression of mitochondrial fatty acid transport genes. This sudden surge in mitochondrial substrate oxidation resulted in higher superoxide production: the avUCP expression at 6 h after heat stress might have not been large enough to alleviate the overproduction of reactive oxygen species (ROS) even though a small amount of endogenous FFA, a potential uncoupler, might have been present in the mitochondria. Thereafter, avUCP content was downregulated while substrate oxidation returned to control levels. This downregulation of avUCP may have caused increased mitochondrial superoxide production, keeping the superoxide production high in the later stages of heat stress. These results suggest that overproduction of mitochondrial ROS in chicken skeletal muscle under the heat stress might result from enhanced substrate oxidation and downregulation of avUCP in a time-dependent manner. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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