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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.
Highlights
In trans-plasma membrane electron transport, electrons from cytosolic donors cross the plasma membrane, resulting in the reduction of extracellular oxidants; this process can occur via shuttle-based electron transport or be mediated by enzyme activity [1,2,3]. tPMET has been shown in a variety of cell types, including epithelial and smooth muscle cells, neurons, and erythrocytes [4].In endothelial cells, tPMET activity reduces extracellular substrates
Primary Myotubes, and Isolated Mouse SOL and extensor digitorum longus (EDL) Are Capable of tPMET
EDL were capable of tPMET, the membrane impermeable electron acceptors water soluble tetrazolium salt 1 (WST-1) and DPIP were
Summary
It does this by using electrons from intracellular reduced nicotinamide adenine dinucleotide (NADH) to blood-borne electron acceptors, resulting in an influence on vascular and organ function, as well as blood composition [4]. TPMET aids in maintaining redox homeostasis [5], meaning a balance between an oxidative environment and a reducing environment This is beneficial, because it has been reported that an unbalanced redox state has been implicated as one of the primary factors leading to obesity-associated complications including types of metabolic dysfunction such as diabetes [6]. The ascorbate recycling process involves export of ascorbate via gap-junctions, volume-sensitive (VSOAC) and
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