{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T13:18:52Z","timestamp":1765545532788,"version":"build-2065373602"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2008,12,23]],"date-time":"2008-12-23T00:00:00Z","timestamp":1229990400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2009,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cyclophosphamide (CP) is an antineoplastic agent that is used for the treatment of many neoplastic diseases. Hemorrhagic cystitis (HC) is a major dose limiting side effect of CP. Recent studies show that aminogaunidine, an inhibitor of inducible nitric oxide synthase is a potent antioxidant and prevents changes caused by oxidative stress such as depletion of antioxidant activity and tissue injury. The purpose of the study is to investigate the effect of aminoguanidine on parameters of oxidative stress, antioxidant enzymes and bladder injury caused by CP. Adult male rats were randomly divided into four groups. Control rats were administered saline; the AG control group received 200\u2009mg\/kg body wt of aminoguanidine; The CP group received a single injection of CP at the dose of 150\u2009mg\/kg body wt intraperitoneally. The CP\u2009+\u2009AG group received aminoguanidine (200\u2009mg\/kg body wt) intraperitoneally 1\u2009h before the administration of CP. The rats were sacrificed 16\u2009h after CP\/saline administration. The bladder was used for light microscopic studies and biochemical studies. The markers of oxidative damage including protein carbonyl content, protein thiol, malondialdehyde and conjugated dienes were assayed in the homogenates along with the activities of the antioxidant enzymes, superoxide dismutase, glutathione peroxidase, catalase, and glutathione reductase and glutathione <jats:italic>S<\/jats:italic> transferase. In the bladders of CP treated rats edema of lamina propria with epithelial and sub\u2010epithelial hemorrhage was seen. All the parameters of oxidative stress that were studied were significantly elevated in the bladders of CP treated rats. The activities of the antioxidant enzymes were significantly lowered in the bladders of CP treated rats. Aminoguanidine pretreatment prevented CP\u2010induced oxidative stress, decrease in the activities of anti\u2010oxidant enzymes and reduced bladder damage. The results of the present study suggest the antioxidant role for aminoguanidine in CP\u2010induced bladder damage. 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