Objective   To explore the role and significance of free radicle in the pathophsiological mechanisms of diabetic cystopathy (DCP).     Methods   The detrusor strip contraction experiments were performed and observed in the group of type 2 diabetes mellitus (T2DM) rats at different time stages and the control group. The bladder tissue samples was made into homogenate

and the activities of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA) were determined.     Results   The minimum stretch forces to induce the detrusor contractions in T2DM group were larger than the control group. Compared with the control group

the detrusor contractive frequency was higher in the period of 0 to 16 weeks

but was lower after the 20th week. The maximum detrusor contractive forces in the T2DM group showed a descended tendency with the elapse of the experiment time. In the bladder homogenate of the control group

the activities of SOD was declined after reaching the peak at the stage of 8th week

and then escalated at the stage of 24th week. As for the T2DM group

the activities of SOD became higher in the 4th week

than descended at the stage of 8th and 24th weeks. The contents of MDA in both groups showed descended tendency. In T2DM group

MDA became even lower than the control group in the 4th week and became higher than the control group in the 8th week. The ratio of SOD/MDA in T2DM group was lower than the control group. In details

the ratio of SOD/MDA in T2DM group rose significantly in the 4th week

while declined in the 8th week. There was a negative correlation between the maximum detrusor contractive force and detrusor contractive frequency

and a positive correlation between the maximum detrusor contractive force and the contents of MDA.     Conclusion   The destrusor functions are impaired  by Diabetes Mellitus. In the initial stage of DCP

the bladder functions are normal

because the detrusor had a high ability to remove the free radicle. In the progression stage of DCP

the bladder functions become decompensation

because the organism is seriously injured by the free radicle. So the impairment by free radicle is one of important mechanisms of destrusor impairment of diabetic cystopathy.