Diabetes mellitus affects skeletal muscle and free radicals may be implicated in the manifestation of diabetes complications. The present study investigated effects of alpha-tocopherol on diabetic dorsiflexor muscle via recording resting membrane potentials (RMPs), endplate potentials (EPPs), miniature endplate potentials (MEPPs) and isometric twitch tensions. Forty mice were divided randomly into two groups (n=20). One group served as control and the other was injected once with streptozotocin (STZ) solution (60 mg/kg, i.p) to induce diabetes. The animals were then divided further into two subgroups (n = 10). Alpha-tocopherol (100 mg/kg, i.p) was administered daily to one control and one diabetic group for 3 weeks prior to recording day. Experiments were conducted 4 weeks following diabetes induction. Isometric twitch tension was measured in anaesthetized mice (2 mg/g urethane, i.p) via a transducer connected to a computer system. Resting membrane potentials and MEPPs were measured by utilizing the intracellular recording method. Compared to control, diabetic mice showed reduced twitch tension (4.4 ± 0.4 g control vs. 2.5 ± 0.3 g diabetic) and demonstrated delayed half time of decay. Diabetic flexor muscle also displayed significant reduction in MEPPs frequencies with no changes in RMPs. Alpha-tocopherol reversed tension reduction in diabetic mice (from 2.5 ± 0.3 to 3.8 ± 0.4 g), impacted delayed half time of decay and reversed reduction in MEPPs frequencies. Alpha-tocopherol exerts a protective role against diabetes-induced peripheral muscle dysfunction. This effect is probably mediated via a free radical scavenging mechanism or modification of Ca2+ homeostasis.
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