CONCLUSIONS: Genetic deletion of NADPH-oxidase subunitprevented eNOS uncoupling and ROS generation in BMT sicklep47phox�/� KO mice. Moreover, BMT sickle p47phox�/� KO micedo not exhibit a priapism phenotype associated with sickle cell disease.These data suggest that NADPH-oxidase activation is a key molecularevent contributing to NO imbalance in sickle cell disease-associatedpriapism.

Source of Funding: NIH, AUA Foundation MD/PhD Fellowship

916APOCYNIN IMPROVES ERECTILE FUNCTION IN DIABETIC RATSTHROUGH REGULATION OF NADPH OXIDASE EXPRESSION

Mingchao Li, Bo Hu, Tao Wang, Ke Rao, Jun Yang, Jihong Liu*,Zhangqun Ye, Wuhan, China, People’s Republic of

INTRODUCTION AND OBJECTIVES: The goal of this experi-ment was to test the hypothesis that NADPH oxidase inhibitor apocynincan ameliorate diabetes-related ED.

METHODS: The diabetic rats were treated with or without theNADPH oxidase inhibitor apocynin in the drinking water. Erectileresponses were evaluated by determining mean arterial blood pres-sure (MAP) and intracavernosal pressure (ICP) with electrical stim-ulation of the cavernous nerve. mRNA expression levels were meas-ured by Real-time polymerase chain reaction (PCR). Proteinsexpression levels were examined by Western blot. Reactive OxygenSpecies (ROS) productions were measured by dihydroethidium(DHE) stainning.

RESULTS: The ratio of Maximum ICP-to-MAP (MaxICP/MAP)was significantly decreased in diabetic ED rats compared to that ofage-matched control rats (P�0.05), apocynin increase the erectilefunction in diabetic rats (P�0.05). RhoA (cytosol), nNOS, eNOS ex-pressions were reduced, when compared to that of control rats(P�0.05), apocynin significantly elevated the expression levels of themin diabetic rats (P�0.05). ROCK1, RhoA (membance), p-MYPT1 andNADPH oxidase subunit p47phox and p67phox expressions wereincreased in diabetic rats when compared to that of control rats(P�0.05), apocynin significantly reduced the expression levels of themin diabetic rats (P�0.05). ROS productions were increased in diabeticrats when compared to that of control rats (P�0.05), apocynin signifi-cantly reduced the ROS productions in diabetic rats (P�0.05).

CONCLUSIONS: NADPH oxidase inhibitor apocynin can ame-liorate diabetes-related ED by inhibiting the overactivity of NADPHoxidase and RhoA/ROCK signaling pathway.

Source of Funding: This work was supported by grant fromNational Natural Sciences Foundation of China (No. 81070484)

917COMBATING COUNTERFEITING: THE CAMPAIGN AGAINSTCOUNTERFEIT PDE5 INHIBITORS

Dorsey, Jr. Philip*, Wayne Hellstrom, New Orleans, LA

INTRODUCTION AND OBJECTIVES: Counterfeit medicationspose significant health risks due to variable concentrations of activepharmaceutical ingredient, inappropriate active ingredients and un-known contaminants. Due to the reluctance of men to seek medicaltreatment for erectile dysfunction (ED), phosphodiesterase type 5 in-hibitors (PDE5i) are a prime target for counterfeiting. Sildenafil is themost counterfeited medication produced by Pfizer. In response to therisks of counterfeit sildenafil, Pfizer has implemented a successfulcampaign consisting of patient education, the use of novel technologyand collaboration with law enforcement to prevent these counterfeitsfrom reaching patients. These efforts have led to rising yearly seizuresof counterfeit sildenafil and is an example of an effective strategy toaddress a growing market for counterfeit medications.

METHODS: A PUBMED search for the key words “counterfeitPDE5i” was performed and publications from the FDA and WHOmentioning counterfeit sildenafil were reviewed. Pfizer provided data onseizures of sildenafil tablets.

RESULTS: In 2009, more than 11 million dosages of counterfeitPfizer medicines were seized; 88% were counterfeit sildenafil. Between2006 and 2009, counterfeit seizures increased 37%, 31% increase incounterfeit sildenafil. Between May 2005 and July 2009, 2383 sus-pected counterfeit sildenafil tablets were seized in Europe, the MiddleEast and Africa and sent to Pfizer for analysis; 82% were counterfeit.76% of the 483 sildenafil tablets obtained during online monitoring byPfizer were counterfeit.

CONCLUSIONS: Sildenafil is one example in the growingcounterfeit medication market. Significant investment by manufacturesin patient education on the risks of counterfeit drugs, prudent use ofonline pharmacies and innovative packaging technologies to identifycounterfeit tablets and close collaboration with law enforcement repre-sent four essential components of an effective campaign against coun-terfeit medications. The foundation of these efforts, however, lies withindividual healthcare providers who can directly address this issuethrough educating their patients on potential for exposure to counterfeitsildenafil when purchasing “generic” medications from unregulatedsources and when using “herbal” supplements. While progress hasbeen made in increasing public awareness on this issue and methodsto remove them from circulation have evolved, continued collabora-tion between manufactures, regulatory bodies, law enforcement andhealthcare providers is needed to combat this important publichealth issue.

Source of Funding: None

918THE MORPHOLOGY AND MOLECULAR EXPRESSION OFDIFFERENT GENES IN THE PROSTATE VENTRAL LOBE OFADULT RATS ARE RESPONSIVE TO A SHORT TIMELEPTIN TREATMENT

Cristiane Ramos*, Rio de Janeiro, Brazil; Jorge Alves-Pereira, SiciliaColli, Francisco Sampaio, rio de janeiro, Brazil

INTRODUCTION AND OBJECTIVES: It is known that leptin hasan important role in regulating the reproductive system besides its mainrole in the regulation of body weight and food intake. The discovery ofleptin synthesis and their receptors expression in the urogenital systemprovide new insights into the pathophysiology of reproduction that has yetto be understood. The aim of this study was to evaluate the effect of a shorttime leptin treatment on the morphology and molecular expression ofdifferent genes in the prostate ventral lobe.

METHODS: Adult male rats were treated (L) with 50 �L of mouserecombinant leptin (80 ng/g BW, sc) or with the same volume of salinesolution (C) for four days at 16:00 hours. Two hours after the last leptininjection all animals were killed. Blood samples were collected to evalua-tion of testosterone by radioimmunoassay. The prostate ventral lobeswere excised, processed and paraffin embedded for morphometric eval-uation using Image J software. The lobes were also kept at �80C foranalysis of aromatase, androgen and estrogen beta receptors, short andlong leptin receptors, and leptin expression by real time PCR. Statisticalsignificance was determined by student’s t-test.

RESULTS: Morphometric analysis showed that the leptin treat-ment led to a significant reduction on cell density, lumen acini’s area andtotal acini area while the epithelial height and acini number were signifi-cantly increased (figure 1). The leptin treatment also resulted in a signifi-cant increase in the expression of all genes studied (figure 2). Thetestosterone serum level was significantly reduced (C�1.62�0.4 andL�0.57�0.15, p�0.03).

CONCLUSIONS: The present data suggest that a short time leptintreatment can alters the morphology of the prostate ventral lobe of adultrats possibly by reducing testosterone serum level and increasing geneexpression of several genes that are important for prostate function andmorphology.

Vol. 185, No. 4S, Supplement, Monday, May 16, 2011 THE JOURNAL OF UROLOGY� e367