Abstract
Correction: Crucial Role of Membrane Potential in Heat Stress-Induced Overproduction of Reactive Oxygen Species in Avian Skeletal Muscle Mitochondria
Highlights
Oxidative stress resulting from an imbalance between antioxidative capacity and reactive oxygen species (ROS) generation, is associated with many pathological processes, neurodegenerative diseases and ageing [1]
It can be appreciated that the H2O2 production rate at the furthest point to the right in each kinetic curve was appreciably higher for the heat-stressed group than for the control group, which suggests that mitochondria isolated from the heat-stressed group may have an increased DY in state 4 compared to that of controls (Fig. 2A)
The present study confirms that acute heat stress induces mitochondrial ROS production, resulting in skeletal muscle oxidative damage in birds exposed to such conditions
Summary
Oxidative stress resulting from an imbalance between antioxidative capacity and reactive oxygen species (ROS) generation, is associated with many pathological processes, neurodegenerative diseases and ageing [1]. We have previously found that acute heat stress stimulates mitochondrial ROS production [9], causing oxidative damage to the skeletal muscle of birds [6]. We previously reported that mitochondrial ROS production in heatstressed birds was significantly increased when mitochondria were energized with succinate as a complex II-linked substrate [16,17]; this was accompanied by an increase in mitochondrial DY [16,17]. There is no direct evidence regarding the dependence of ROS overproduction on DY in the skeletal muscle mitochondria of acute heat-stressed birds. We reported that mitochondrial ROS production with glutamate/malate as complex I-linked substrates was increased by heat exposure [9,18,19], but it remains unclear if the overproduction of ROS depends on the magnitude of DY
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