Oxidative stress plays a role in diabetes-induced bladder dysfunction in a rat model.
OBJECTIVE
To evaluate the oxidative status of the bladder 8 weeks after diabetes induction. Oxidative stress has recently been implicated in the pathogenesis of diabetes complications, but its role in diabetic cystopathy has not been studied.


METHODS
Sprague-Dawley rats were divided into three groups: control (n = 11), diuretic control (5% sucrose drink; n = 6), and streptozotocin-induced diabetic group (n = 14). Eight weeks later, the bladders were dissected. We measured the antioxidant scavenging enzymes (catalase and superoxide dismutase)-like activity and the levels of the thiobarbituric acid reactive substances, as a marker of lipid peroxidation. We also examined the levels of inducible nitric oxide synthase and apoptosis in the bladders.


RESULTS
We found a statistically significant reduction in the catalase-like activity in the bladders from the diabetic group compared with the other groups (P = 0.017, diabetic versus control); the difference in the superoxide dismutase-like activity was not statistically significant among the groups. The thiobarbituric acid reactive substances levels were significantly greater in the diabetic compared with other groups (131.9 +/- 47.5, 46.7 +/- 17.9, and 60.9 +/- 25.4 nmol/mg protein in the diabetic, control, and diuretic group, respectively, P = 0.006, diabetic versus control). Immunohistochemical and apoptosis studies showed a statistically significant increased number of inducible nitric oxide synthase-positive cells and apoptotic cells in the diabetic bladder smooth muscle cells (P <0.001).


CONCLUSIONS
Our findings showed that oxidative stress occurred in the bladders of the STZ-diabetic rats and was not mediated by diuresis. The oxidative damage of the smooth muscle cells may be a contributory factor in diabetic cystopathy.
Beshay
Evette
E
Department of Urology, McGill University, Montreal, Quebec, Canada.
Carrier
Serge
S
D000818:Animals; D017209:Apoptosis; D002374:Catalase / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D015227:Lipid Peroxidation; D008297:Male; D009130:Muscle, Smooth / Q000503:physiopathology; D019001:Nitric Oxide Synthase / Q000032:analysis; D052247:Nitric Oxide Synthase Type II; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000032:analysis; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D013997:Time Factors; D001743:Urinary Bladder / Q000503:physiopathology; D001745:Urinary Bladder Diseases / Q000201:enzymology / Q000209:etiology*
D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D013482:Superoxide Dismutase