Diabetes induces hyperglycemia which disrupts the intracellular redox balance, by increasing the production of reactive oxygen species and reducing tissue antioxidant concentrations. Glutathione (GSH) is a key intracellular antioxidant in skeletal muscle. Previous studies in our laboratory have shown that irradiation for 18d with near-red light (670 nm) attenuates oxidative stress in a Type I diabetic animal model. PURPOSE: The purpose of this study was to examine the difference in oxidative stress in red and white portions of the gastrocnemius muscle (RG and WG, respectively) after acute and chronic treatments with NIR on type I diabetes. METHODS: Male Wistar rats were randomly assigned to one of three treatment groups: Untreated Control (CON), Streptozotocin-treated non-light exposed rats (STZ) and STZ-treated rats exposed to 670 nm NIR-LED PBM (NIR). Streptozotocin was administered at a dose of 50 mg/kg (ip) on day 0. Rats were placed in a plexiglass restraint and exposed to NIR (670 nm) treatment at an intensity of 50 mW/cm2 for 5 minutes (surface energy density: 15 J/cm2). Animals were treated once per day, 5 days (d) per week from d0 to d18 in the acute study and from d3 to d98 in the chronic study. Animals were euthanized, perfused with saline and then the RG and WG sections were rapidly dissected, flash frozen, stored at -80° C. Tissues were analyzed for total GSH (GSHT), reduced GSH (GSHR) and oxidized GSH (GSSG) using a commercial kit (Cayman Biochemical). ANOVAs and t-tests were run; significance was p < 0.05. RESULTS: In the acute study there were no differences in GSH redox status in WG or RG muscle. However, in the chronic study STZ-treatment profoundly increased the GSSG/GSH ratio in WG muscle and NIR treatment restored the GSSG/GSHR ratio to control values in WG. CONCLUSIONS: Our data indicate that chronic, but not acute, STZ-induced hyperglycemia reduced oxidative capacity, disrupted glutathione redox status and increased myocyte apoptosis. NIR treatment restored GSH redox status in WG muscle consistent with findings in other degenerative disease models and indicative of an improvement in mitochondrial energy metabolism and protection against antioxidant depletion. (Funding: RGI grant [UWM]; BTA grant [State of Wisconsin]).