Accumulating data support the hypothesis that reactive oxygen species (ROS) play a critical role in the vascular complications observed in diabetes. However, the mechanisms of ROS-mediated vascular complications in diabetes are not clear. Here, we tested the hypothesis that ROS-mediated increase in pro-apoptotic factor bax expression leads to medial smooth muscle cell (SMC) apoptosis which is associated with neointima formation. We used a fructose rich diet for four weeks to model type 2 diabetes in rats. SOD mimetic membrane permeable Tempol (1mM) was administered in drinking water to scavenge superoxide starting one day before surgery and continued during the duration of the experiment. Vascular injury resulted in a significant increase in medial SMC apoptosis which was associated with neointima formation. The number of medial SMC positive for bax immunostaining significantly increased in injured arteries compared to uninjured arteries. Superoxide scavenging by tempol treatment inhibited both the bax positive index as well as the apoptotic index of medial SMC in response to vascular injury. Tempol treatment inhibited apoptotic loss of medial SMC thus increasing their density in the injured arteries. These alterations in the media were associated with a marked decrease in neointima formation in injured arteries. We conclude that bax expression may play an important role in VSM cell apoptosis and finally this regulatory mechanism is redox sensitive.