TY - JOUR
T1 - Effect of heat stress-induced production of mitochondrial reactive oxygen species on NADPH oxidase and heme oxygenase-1 mRNA levels in avian muscle cells
AU - Kikusato, Motoi
AU - Yoshida, Hayami
AU - Furukawa, Kyohei
AU - Toyomizu, Masaaki
N1 - Funding Information:
This work was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan ( 24380147 : M.T.).
Publisher Copyright:
© 2015 Elsevier Ltd.
PY - 2015/8/1
Y1 - 2015/8/1
N2 - Heat stress is a major factor inducing oxidative disturbance in cells. In the present study, we investigated the mechanism of overproduction of reactive oxygen species (ROS) in cultured avian muscle cells in response to heat stress, and also focused attention on the interaction of mitochondrial superoxide anions with altered NADPH oxidase (NOX), superoxide dismutase (SOD) and heme oxygenase-1 (HO-1) mRNA levels in heat-stressed cells. Exposure of cells to heat stress conditions (41. °C, 6. h) resulted in increased mitochondrial superoxide and intracellular ROS levels, and increased carbonyl protein content as compared with that of normal cells (37. °C). The mitochondrial uncoupler 2,4-dinitrophenol lowered intracellular ROS levels in heat-stressed cells. Heat stress increased NOX4 mRNA and decreased HO-1 mRNA levels, while SOD1 and SOD2 mRNA levels remained relatively stable in heat-stressed cells. Addition of the superoxide scavenger 4-hydroxy TEMPO to the culture medium of heat-stressed cells restored mitochondrial superoxide and intracellular ROS levels as well as NOX4 and HO-1 mRNA levels to near-normal values. We suggest that mitochondrial superoxide production could play an influential role in augmenting oxidative damage to avian muscle cells, possibly via the up-regulation of NOX4 and down-regulation of HO-1 in heat-stressed avian muscle cells.
AB - Heat stress is a major factor inducing oxidative disturbance in cells. In the present study, we investigated the mechanism of overproduction of reactive oxygen species (ROS) in cultured avian muscle cells in response to heat stress, and also focused attention on the interaction of mitochondrial superoxide anions with altered NADPH oxidase (NOX), superoxide dismutase (SOD) and heme oxygenase-1 (HO-1) mRNA levels in heat-stressed cells. Exposure of cells to heat stress conditions (41. °C, 6. h) resulted in increased mitochondrial superoxide and intracellular ROS levels, and increased carbonyl protein content as compared with that of normal cells (37. °C). The mitochondrial uncoupler 2,4-dinitrophenol lowered intracellular ROS levels in heat-stressed cells. Heat stress increased NOX4 mRNA and decreased HO-1 mRNA levels, while SOD1 and SOD2 mRNA levels remained relatively stable in heat-stressed cells. Addition of the superoxide scavenger 4-hydroxy TEMPO to the culture medium of heat-stressed cells restored mitochondrial superoxide and intracellular ROS levels as well as NOX4 and HO-1 mRNA levels to near-normal values. We suggest that mitochondrial superoxide production could play an influential role in augmenting oxidative damage to avian muscle cells, possibly via the up-regulation of NOX4 and down-regulation of HO-1 in heat-stressed avian muscle cells.
KW - Mitochondrial membrane potential
KW - Protein degradation
KW - Superoxide anion
KW - Superoxide dismutase
KW - Uncoupling protein
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U2 - 10.1016/j.jtherbio.2015.04.005
DO - 10.1016/j.jtherbio.2015.04.005
M3 - Article
C2 - 26267493
AN - SCOPUS:84928883288
SN - 0306-4565
VL - 52
SP - 8
EP - 13
JO - Journal of Thermal Biology
JF - Journal of Thermal Biology
ER -