Abstract
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.
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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