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Biomedical subjects

Hamit Okur

Publications and source records attributed to Hamit Okur.

4 recordsLinked to original sources
PubMed2006

Effects of prenatal flutamide on testicular development, androgen production and fertility in rats.

INTRODUCTION: To investigate the effects of blocking prenatal androgen with the anti-androgen flutamide on testicular weight (TW), seminiferous tubular diameter (STD), testicular biopsy score (TBS), testicular testosterone (TT), and fertility. MATERIALS AND METHODS: Ten pregnant Wistar albino rats were injected with flutamide (100 mg/kg) on gestational days 16 and 19. Rats injected with the solvent were used as controls. Male pups from these dams were evaluated for testicular descent on postnatal day 22. The ability of each male to produce offspring was tested when the animals were aged 130 days. The rats were killed when 180 days old, and the testes were removed. RESULTS: Sixteen of the 24 male rats (66.6%) exhibited cryptorchidism (6 unilateral, 10 bilateral) in the flutamide-treated group. Three of the rats with normally descended testicles were fertile, but none of the cryptorchid rats was fertile in flutamide-treated group. The average TW, mean STD, TBS and TT levels of the flutamide-treated rats was significantly lower than in the solvent-injected rats. However, there was no significant difference in these values between descended and undescended testes in flutamide-treated rats. CONCLUSION: Blocking of prenatal androgen with flutamide interferes with testicular development by inhibiting testicular descent, and also effects testicular morphology and function in both the descended and undescended testes of rats.

Androgen Antagonists↗
PubMed2005

Renal effects of long-term leptin infusion and preventive role of losartan treatment in rats.

BACKGROUND: Leptin has direct and indirect effects on renal pathophysiological characteristics. In the present study, the effects of long-term leptin infusion on the renal hemodynamics, renal excretory functions, and the expression of transforming growth factor-beta (TGF-beta), plasma endothelin-1 (ET-1) levels, and preventive effects of the angiotensin II type 1 receptor antagonist, losartan, on these renal changes were evaluated. METHODS: The study was performed by using forty Wistar albino rats. On day 0, osmotic mini-pumps filled with leptin or placebo were intraperitoneally placed under sterile conditions. The rats in Group L (Leptin group, n=15) and Group LL (Leptin-losartan group, n=15) were given recombinant murine leptin at a rate of 250 ng per hour for 28 days. Control rats (Group C, n=10) were administered placebo at the same infusion rate. The rats in Group LL were also administered losartan (10 mg kg(-1) d(-1)) perorally for 28 days. On day 28, the rats were placed in metabolic cages, and the food and water intakes were determined, and the urine was collected for 24 h. At the end of the study, systolic blood pressure (SBP), diastolic blood pressure (DBP) were determined directly from the left femoral artery, and renal blood flow (RBF) was recorded indirectly using a laser Doppler flow module. RESULTS: Leptin infusion did not produce any changes in systemic arterial blood pressures and urinary flow rate. The rates of creatinine (Cr), sodium (Na), and protein excretions of the animals infused leptin were significantly increased. The urinary Cr and Na excretions were decreased, while the urinary protein excretion was normalized with the losartan treatment. The rats infused leptin had also higher circulating ET-1 levels. ET-1 levels were also reversed to the normal values with the losartan treatment. Renal TGF-beta1 expression was determined immunohistochemically, and it was more prominent in the renal tubules from the rats treated with leptin. The losartan treatment had no effect on renal TGF-beta1 expression. CONCLUSIONS: Our results indicate that pathophysiological increases in plasma leptin concentrations cause enhanced renal Na, Cr and protein excretions, and high circulating ET-1 levels. Na and Cr excretions were decreased, while proteinuria and plasma ET-1 levels were normalized by losartan treatment, suggesting that renin-angiotensin system activation may have a role in leptin induced renal changes. TGF-beta1 may have an important role in leptin induced nephropathy.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2003

The role of infection and free oxygen radical damage in reflux nephropathy: an experimental study.

PURPOSE: We compared the effects of sterile and infected urine on reflux nephropathy in rabbits with experimental vesicoureteral reflux. MATERIALS AND METHODS: We used 2-month-old male New Zealand rabbits in this study. Group 1 (5 rabbits) served as the control, group 2 (7) was the vesicoureteral reflux plus sterile urine group and group 3 (8) was the reflux plus infected urine group. Cystography and 99mTc-dimercapto-succinic acid renal scintigraphy were performed before the reflux procedure. To create unilateral vesicoureteral reflux the roof of the right intravesical ureter was incised. Escherichia coli suspension (2 ml.), 105 E. coli in 1 ml.) was introduced into the bladder in addition to the reflux procedure in group 3. Right vesicoureteral reflux was confirmed by cystography 2 weeks after reflux. Dimercapto-succinic acid scintigraphy was performed at 3 weeks and the animals were sacrificed and examined. Free oxygen radical damage was investigated by measuring malondialdehyde levels in renal tissue. ANOVA and Scheffe's test were used for statistical analysis. RESULTS: Histopathological evaluation of the right kidney from group 2 rabbits showed mild interstitial fibrosis and mononuclear cell infiltration. The right kidney from group 3 rabbits showed apparent periglomerular fibrosis, tubular atrophy and dilatation, severe interstitial scarring and fibrosis with mononuclear cell infiltrate. There were marked histopathological changes in the right kidney of group 3 rabbits. The absolute percent dose uptake was unchanged in group 2 rabbits (p >0.05). There was significantly decreased uptake in refluxing kidneys and increased uptake in the contralateral nonrefluxing kidneys after vesicoureteral reflux in group 3 rabbits. The malondialdehyde level in the right renal tissue of group 3 was significantly higher than that in controls and in group 2 (p <0.05). The malondialdehyde level in the sterile reflux group did not differ significantly from that in the control group (p >0.05). CONCLUSIONS: The results of this study show that free oxygen radical damage in the presence of infection has an important role in reflux nephropathy.

Animals↗