Vitamin D is known to have a biological role in many extra skeletal tissues in the body including muscle. Vitamin D deficiency has been associated with preferential atrophy of type II fibres in human muscle. Vitamin D at physiological concentrations has been reported to protect cells against oxidative damage. In this study we examined whether vitamin D deficiency induces muscle oxidative stress in a rat model and further if pre or post treatment of C2C12 muscle cells with vitamin D offers protection against oxidative stress induced muscle proteolysis. For in vivo studies a vitamin D deficient rat model was employed. Vitamin D deficient rats were fed a diet devoid of vitamin D, while control rats were given the same diet containing 1000IU vitamin D3/Kg diet. For in vitro studies the C2C12 mouse myoblast cell line was used. Protein carbonylation as a marker of protein oxidation was significantly increased in both the deficient muscle and vehicle-treated C2C12 cells (P<0.01). Vitamin D deficiency led to an increase in activities of the glutathione-dependent enzymes and decrease in SOD and catalase enzymes in the rat muscle(P<0.001). Higher nitrate levels indicative of nitrosative stress was observed in the deficient muscle compared to control muscle(P<0.01). Rehabilitation with vitamin D could reverse the alterations in oxidative and nitrosative stress parameters.  Increase in total protein degradation, 20S proteasomal enzyme activity, muscle atrophy gene markers(Atrogin & MuRF) and expression of proteasome subunit genes(PSC2 & PSC8) induced by oxidative stress were corrected both by pre/post treatment of C2C12 muscle cells with vitamin D. SOD activity increased in presence of vitamin D(P<0.01).The data presented indicates that vitamin D deficiency leads to mild oxidative stress in the muscle which may act as a trigger for increased proteolysis in the vitamin D deficient muscle.