Abstract
There is increasing interest in the effect of energy metabolism on oxidative stress, but much ambiguity over the relationship between the rate of oxygen consumption and the generation of reactive oxygen species (ROS). Production of ROS (such as hydrogen peroxide, H2O2) in the mitochondria is primarily inferred indirectly from measurements in vitro, which may not reflect actual ROS production in living animals. Here, we measured in vivo H2O2 content using the recently developed MitoB probe that becomes concentrated in the mitochondria of living organisms, where it is converted by H2O2 into an alternative form termed MitoP; the ratio of MitoP/MitoB indicates the level of mitochondrial H2O2 in vivo. Using the brown trout Salmo trutta, we tested whether this measurement of in vivo H2O2 content over a 24 h-period was related to interindividual variation in standard metabolic rate (SMR). We showed that the H2O2 content varied up to 26-fold among fish of the same age and under identical environmental conditions and nutritional states. Interindividual variation in H2O2 content was unrelated to mitochondrial density but was significantly associated with SMR: fish with a higher mass-independent SMR had a lower level of H2O2. The mechanism underlying this observed relationship between SMR and in vivo H2O2 content requires further investigation, but may implicate mitochondrial uncoupling which can simultaneously increase SMR but reduce ROS production. To our knowledge, this is the first study in living organisms to show that individuals with higher oxygen consumption rates can actually have lower levels of H2O2.
Highlights
Oxidative stress occurs when the generation of reactive oxygen species (ROS) exceeds the capacity of antioxidant defence and repair mechanisms, thereby generating oxidative damage to lipids, DNA and proteins [1]
MitoP/MitoB ratios were independent of mitochondrial density, regardless of whether this was quantified in terms of c oxidase (COX) activity (F1,30.14 1⁄4 1.78, p 1⁄4 0.19) or Citrate synthase (CS) activity (F1,25.17 1⁄4 0.20, p 1⁄4 0.66)
Lett. 11: 20150538 the H2O2 generated by mitochondria during aerobic respiration and that scavenged by antioxidants such as mitochondrial glutathione peroxidase (GPx) [1,3]
Summary
Oxidative stress occurs when the generation of reactive oxygen species (ROS) exceeds the capacity of antioxidant defence and repair mechanisms, thereby generating oxidative damage to lipids, DNA and proteins [1]. Most of the ROS present in cells are produced within the mitochondria as natural by-products of aerobic respiration [1] This has led to the pervasive idea that increased energy expenditure towards one life-history trait will result in greater ROS production, leading to accelerated senescence [4,5,6]. It is still unclear whether higher aerobic respiration alters in vivo ROS levels [7,8].
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