Nrf2 mediates redox adaptations to exercise

Done, Aaron J.; Traustadóttir, Tinna

doi:10.1016/j.redox.2016.10.003

Cited by 219 publications

(191 citation statements)

References 83 publications

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“…The fact that aerobic training reduces oxidative stress is not surprising: the training protocol used in the present study (Figure 1) was indeed demonstrated to increase aerobic capacity and to counteract protein and lipid oxidative modifications in skeletal muscles of heart failure-bearing animals [34]. In addition, many investigators have reported that exercise training boosts antioxidant defenses [33,34,[72][73][74] while decreasing lipid peroxidation [29] and oxidative modifications to proteins and RNA [55]. groups of mice (Table 1) and allowed to determine differences caused by adaptation of muscle to lack of CASQ1 (control CASQ1-null versus WT) and to training (control versus trained CASQ1-null).…”

Section: Protection From Oxidative Stress and Damagesupporting

confidence: 61%

Aerobic Training Prevents Heat-Strokes in Calsequestrin 1 Knockout Mice by Reducing Oxidative Stress

Guarnier

Serano

Michelucci

et al. 2018

Biophysical Journal

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Calsequestrin-1 knockout (CASQ1-null) mice suffer lethal episodes when exposed to strenuous exercise and environmental heat, crises known as exertional/environmental heatstroke (EHS). We previously demonstrated that administration of exogenous antioxidants (N-acetylcysteine and trolox) reduces CASQ1-null mortality during exposure to heat. As aerobic training is known to boost endogenous antioxidant protection, we subjected CASQ1-null mice to treadmill running for 2 months at 60% of their maximal speed for 1 h, 5 times/week. When exposed to heat stress protocol (41°C/1 h), the mortality rate of CASQ1-null mice was significantly reduced compared to untrained animals (86% versus 16%). Protection from heatstrokes was accompanied by a reduced increase in core temperature during the stress protocol and by an increased threshold of response to caffeine of isolated extensor digitorum longus muscles during in vitro contracture test. At cellular and molecular levels, aerobic training (i) improved mitochondrial function while reducing their damage and (ii) lowered calpain activity and lipid peroxidation in membranes isolated from sarcoplasmic reticulum and mitochondria. Based on this evidence, we hypothesize that the protective effect of aerobic training is essentially mediated by a reduction in oxidative stress during exposure of CASQ1-null mice to adverse environmental conditions.

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Section: Protection From Oxidative Stress and Damagesupporting

confidence: 61%

Aerobic Training Prevents Heat-Strokes in Calsequestrin 1 Knockout Mice by Reducing Oxidative Stress

Guarnier

Serano

Michelucci

et al. 2018

Biophysical Journal

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“…Nrf2 then binds to antioxidant response element (ARE) in the nucleus, mediating the transcription and expression of several key antioxidant genes, including NQO1, HO1 and GCLC [33][34][35][36]. Here, we showed that the mRNA expression levels of the Nrf2-dependent genes NQO1 (Fig.…”

Section: K6pc-5 Activates Nrf2 Signaling In Neuronal Cellsmentioning

confidence: 89%

“…4E), indicating Nrf2 protein stabilization. The latter is an essential step forNrf2 nuclear translocation and activation [33][34][35][36].…”

Section: K6pc-5 Activates Nrf2 Signaling In Neuronal Cellsmentioning

confidence: 99%

K6PC-5 Activates SphK1-Nrf2 Signaling to Protect Neuronal Cells from Oxygen Glucose Deprivation/Re-Oxygenation

Liu

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: New strategies are required to combat neuronal ischemia-reperfusion injuries. K6PC-5 is a novel sphingosine kinase 1 (SphK1) activator whose potential activity in neuronal cells has not yet been tested. Methods: Cell survival and necrosis were assessed with a Cell Counting Kit-8 assay and lactate dehydrogenase release assay, respectively. Mitochondrial depolarization was tested by a JC-1 dye assay. Expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling components were examined by quantitative real-timePCR and western blotting. Results: K6PC-5 protected SH-SY5Y neuronal cells and primary murine hippocampal neurons from oxygen glucose deprivation/re-oxygenation (OGDR). K6PC-5 activated SphK1, and SphK1 knockdown by targeted short hairpin RNA (shRNA) almost completely abolished K6PC-5-induced neuronal cell protection. Further work showed that K6PC-5 inhibited OGDR-induced programmed necrosis in neuronal cells. Importantly, K6PC-5 activated Nrf2 signaling, which is downstream of SphK1. Silencing of Nrf2 by targeted shRNA almost completely nullified K6PC-5-mediated neuronal cell protection against OGDR. Conclusion: K6PC-5 activates SphK1-Nrf2 signaling to protect neuronal cells from OGDR. K6PC-5 might be a promising neuroprotective strategy for ischemia-reperfusion injuries.

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“…However, ubiquinol is a particular molecule endowed with both antioxidant properties but also critical for mitochondrial bioenergetics. Recent reports have highlighted that differently from other antioxidants, ubiquinol is able to promote Nrf2 translocation and hence to increase positive stimuli following physical exercise, while inhibiting the NFkB inflammatory pathway [65,[73][74][75].…”

Section: Discussionmentioning

confidence: 99%

Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes

et al. 2018

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Objectives: Physical exercise significantly impacts the biochemistry of the organism. Ubiquinone is a key component of the mitochondrial respiratory chain and ubiquinol, its reduced and active form, is an emerging molecule in sport nutrition. The aim of this study was to evaluate the effect of ubiquinol supplementation on biochemical and oxidative stress indexes after an intense bout of exercise. Methods: 21 male young athletes (26 + 5 years of age) were randomized in two groups according to a double blind cross-over study, either supplemented with ubiquinol (200 mg/day) or placebo for 1 month. Blood was withdrawn before and after a single bout of intense exercise (40 min run at 85% maxHR). Physical performance, hematochemical parameters, ubiquinone/ubiquinol plasma content, intracellular reactive oxygen species (ROS) level, mitochondrial membrane depolarization, paraoxonase activity and oxidative DNA damage were analyzed. Results: A single bout of intense exercise produced a significant increase in most hematochemical indexes, in particular CK and Mb while, on the contrary, normalized coenzyme Q 10 plasma content decreased significantly in all subjects. Ubiquinol supplementation prevented exercise-induced CoQ deprivation and decrease in paraoxonase activity. Moreover at a cellular level, in peripheral blood mononuclear cells, ubiquinol supplementation was associated with a significant decrease in cytosolic ROS while mitochondrial membrane potential and oxidative DNA damage remained unchanged. Discussion: Data highlights a very rapid dynamic of CoQ depletion following intense exercise underlying an increased demand by the organism. Ubiquinol supplementation minimized exerciseinduced depletion and enhanced plasma and cellular antioxidant levels but it was not able to improve physical performance indexes or markers of muscular damage.

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Nrf2 mediates redox adaptations to exercise

Cited by 219 publications

References 83 publications

Aerobic Training Prevents Heat-Strokes in Calsequestrin 1 Knockout Mice by Reducing Oxidative Stress

Aerobic Training Prevents Heat-Strokes in Calsequestrin 1 Knockout Mice by Reducing Oxidative Stress

K6PC-5 Activates SphK1-Nrf2 Signaling to Protect Neuronal Cells from Oxygen Glucose Deprivation/Re-Oxygenation

Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes

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