Crucial role of membrane potential in heat stress-induced overproduction of reactive oxygen species in avian skeletal muscle mitochondria.
Crucial role of membrane potential in heat stress-induced overproduction of reactive oxygen species in avian skeletal muscle mitochondria.
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DOI:
10.1371/journal.pone.0064412
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Toyomizu M
中科院分区:
文献类型:
--
作者:
Kikusato M;Toyomizu M
Heat stress is an environmental factor that causes oxidative stress. We found previously that acute heat stress stimulates the production of reactive oxygen species (ROS) in the skeletal muscle mitochondria of birds, and that this was accompanied by an increase of the mitochondrial membrane potential (ΔΨ) due to increased substrate oxidation by the electron transport chain. We also showed that avian uncoupling protein (avUCP) expression is decreased by the heat exposure. The present study clarifies whether ΔΨ is a major determinant of the overproduction of ROS due to acute heat stress, and if the decrease in avUCP expression is responsible for the elevation in ΔΨ. Control (24°C) and acute heat-stressed (34°C for 12 h) birds exhibited increased succinate-driven mitochondrial ROS production as indicated by an elevation of ΔΨ, with this increase being significantly higher in the heat-stressed group compared with the control group. In glutamate/malate-energized mitochondria, no difference in the ROS production between the groups was observed, though the mitochondrial ΔΨ was significantly higher in the heat-stressed groups compared with the control group. Furthermore, mitochondria energized with either succinate/glutamate or succinate/malate showed increased ROS production and ΔΨ in the heat-stressed group compared with mitochondria from the control group. These results suggest that succinate oxidation could play an important role in the heat stress-induced overproduction of mitochondrial ROS in skeletal muscle. In agreement with the notion of a decrease in avUCP expression in response to heat stress, proton leak, which was likely mediated by UCP (that part which is GDP-inhibited and arachidonic acid-sensitive), was reduced in the heat-exposed group. We suggest that the acute heat stress-induced overproduction of mitochondrial ROS may depend on ΔΨ, which may in turn result not only from increased substrate oxidation but also from a decrease in the mitochondrial avUCP content.
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DOI:
10.1042/bj20081386
发表时间:
2009-01-01
期刊:
The Biochemical journal
影响因子:
--
作者:
Murphy MP
通讯作者:
Murphy MP
DOI:
10.1111/j.1432-1033.1989.tb14867.x
发表时间:
1989-07-01
期刊:
EUROPEAN JOURNAL OF BIOCHEMISTRY
影响因子:
--
作者:
ANDREYEV, AY;BONDAREVA, TO;VYGODINA, TV
通讯作者:
VYGODINA, TV
影响因子:
2.9
作者:
BROWN, RE;JARVIS, KL;HYLAND, KJ
通讯作者:
HYLAND, KJ
影响因子:
4.8
作者:
Goglia, F;Skulachev, VP
通讯作者:
Skulachev, VP
影响因子:
4.4
作者:
Mujahid, A;Yoshiki, Y;Toyomizu, M
通讯作者:
Toyomizu, M