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Antioxidants 2017, 6(4), 89; doi:10.3390/antiox6040089

Trans-Plasma Membrane Electron Transport and Ascorbate Efflux by Skeletal Muscle

1
Department of Biology, Saint Louis University, 3507 Laclede Ave, St. Louis, MO 63103, USA
2
School of Medicine, Saint Louis University, 3507 Laclede Ave, St. Louis, MO 63103, USA
*
Author to whom correspondence should be addressed.
Received: 17 October 2017 / Revised: 7 November 2017 / Accepted: 7 November 2017 / Published: 9 November 2017
(This article belongs to the Special Issue Exercise Induced Muscle Damage and Oxidative Stress)
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Abstract

Trans-plasma membrane electron transport (tPMET) and the antioxidant roles of ascorbate reportedly play a role in protection of cells from damage by reactive oxygen species, which have been implicated in causing metabolic dysfunction such as insulin resistance. Skeletal muscle comprises the largest whole-body organ fraction suggesting a potential role of tPMET and ascorbate export as a major source of extracellular antioxidant. We hypothesized that skeletal muscle is capable of tPMET and ascorbate efflux. To measure these processes, we assayed the ability of cultured muscle cells, satellite cells, and isolated extensor digitorum longus (EDL) and soleus (SOL) to reduce two extracellular electron acceptors, water soluble tetrazolium salt 1 (WST-1), and dichlorophenolindophenol (DPIP). Ascorbate oxidase (AO) was utilized to determine which portion of WST-1 reduction was dependent on ascorbate efflux. We found that muscle cells can reduce extracellular electron acceptors. In C2C12 myotubes and satellite cells, a substantial portion of this reduction was dependent on ascorbate. In myotubes, glucose transporter 1 (GLUT1) inhibitors along with a pan-GLUT inhibitor suppressed tPMET and ascorbate efflux, while a GLUT4 inhibitor had no effect. The adenosine 5′-monophosphate (AMP)-activated protein kinase activator 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) suppressed both tPMET and ascorbate efflux by myotubes, while insulin had no effect. Taken together, our data suggest that muscle cells are capable of tPMET and ascorbate efflux supported by GLUT1, thus illustrating a model in which resting muscle exports electrons and antioxidant to the extracellular environment. View Full-Text
Keywords: tPMET; ascorbate; skeletal muscle; WST-1; GLUT1 tPMET; ascorbate; skeletal muscle; WST-1; GLUT1
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MDPI and ACS Style

Eccardt, A.M.; Bell, T.P.; Mattathil, L.; Prasad, R.; Kelly, S.C.; Fisher, J.S. Trans-Plasma Membrane Electron Transport and Ascorbate Efflux by Skeletal Muscle. Antioxidants 2017, 6, 89.

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