Burak Çimen

The Effect of Testosterone Replacement Therapy on Bladder Functions and Histology in Orchiectomized Mature Male Rats

OBJECTIVE To investigate the effect of testosterone replacement therapy on bladder functions and smooth muscle/collagen content in orchidectomized orchiectomized mature male rats. METHODS The study included 25 mature male Sprague-Dawley rats divided into 3 groups. After bilateral orchiectomy, 8 rats received intramuscular saline injection, as a control group, and 8 rats received intramuscular injection of testosterone undecanoate 100 mg/kg as a treatment group. The sham group had 9 rats. Urodynamic studies were performed in all groups, before and after the study. The rats were killed after 60 days, and cystometric findings and smooth muscle/collagen ratio of the bladders were compared between the groups. RESULTS From the beginning to the end of the experiment, mean maximal bladder capacity increased 46.61% +/- 20.82 in the testosterone treatment group, while decreased 38.91% +/- 17.83 in control group, revealing a significant difference (P = .002). Smooth muscle/collagen ratio was significantly higher in the testosterone treatment group (1.53 +/- .34) than in the control group (1.05 +/- .32), (P = .01). CONCLUSIONS This study showed that bladder capacity and smooth muscle/collagen content improved with testosterone therapy in orchiectomized rats. Therefore, testosterone replacement therapy in late-onset hypogonadal men with urogenital dysfunction may have a positive role to improve bladder function by increasing bladder smooth muscle.

Protective and therapeutic effects of swimming exercise training on diabetic peripheral neuropathy of streptozotocin-induced diabetic rats

Background: Diabetic peripheral neuropathy (DPN) is a typical complication of diabetes. No definitive treatment and prevention of DPN has been established, and very few data on the role of exercise training on DPN have been reported. Aim of the study: The protective and therapeutic effects of aerobic physical activity on the development of DPN in Type 1 were investigated. Methods: Rats were assigned to 5 groups: C (control), E (exercise), D (diabetic), DEx (exercise after diabetic), ExD (diabetic after exercise); C containing 10 animals and E, D, DEx, ExD containing 15 animals. Diabetes was induced with streptozotocin (STZ) (45 mg/kg, ip). Development of diabetes was confirmed by measuring blood glucose levels 2 days after STZ treatment. Body weights of all the animals were evaluated weekly throughout the experiment. Motor dysfunction defined by a significant increase in compound muscle action potential (CMAP) latency was recorded. The amplitude of CMAP which mainly reflects axonal dysfunction was also measured using standard techniques. Sciatic nerve morphometry and blood glucose levels were analyzed in all the groups. Results: Blood glucose level significantly increased 2 days after STZ injection. All diabetic rats showed decreased body weight compared to control rats. An increase in motor latency of CMAP and a decrease in amplitude of CMAP, indicative of neuropathy, were seen in STZ rats. On the completion of the study (the 56th day post-STZ), histological examination revealed significant myelin loss (thinner myelin) in sciatic nerves of STZ rats. Treatment with swimming exercise had no effect on glycemic control but restored body weight, CMAP amplitude, CMAP latency or motor dysfunction in the diabetic animals. Conclusions: This study suggests that swimming exercise training has protective and therapeutic effects on DPN of STZ-induced diabetic rats.

Assessment of Cadmium Genotoxicity in Peripheral Blood and Bone Marrow Tissues of Male Wistar Rats

In this study, Cadmium (Cd) genotoxicity was investigated in both bone marrow and peripheral blood treatment using rat micronucleus technique as genotoxicity test at acute and chronic treatment in the same animals. This study evaluated the frequency of micronuclei in the peripheral blood and bone marrow of male rats treated with unique cadmium dose (15 mg/kg. body w/day) by gavage for 60 days and acute treatment for 24 h, respectively. Mitomycin C (MMC) 2 mg/kg body wt was used as a positive control. This study shows that cadmium chloride treatment significantly induced the frequency of micronucleus in polychromatic erythrocytes in both tibia bone marrow and peripheral blood (p < 0.001, p < 0.01, respectively). This increase in micronucleus frequency shows that cadmium has a genotoxic effect on bone marrow and peripheral blood at this level. Also, in order to determine cytotoxicity in bone marrow and peripheral blood, the ratio of polychromatic erythrocytes to normochromatic erythrocytes was calculated in bone marrow and peripheral blood. Cd treatment decreased this ratio in only bone marrow. The results of this study demonstrate that Cd has both toxic and genotoxic potential in bone marrow and only genotoxic potential in peripheral blood. There is a significant difference between the control group and exposed group, including acute and chronic treatment for blood Cd level (p < 0.001). No significant difference was found between acute and chronic exposure group (p > 0.05).

Effects of venlafaxine and fluoxetine on lymphocyte subsets in patients with major depressive disorder: A flow cytometric analysis

BACKGROUND Studies have yielded conflicting results concerning flow cytometric lymphocyte analyses in patients with depression. Data about the effect of antidepressants on lymphocyte subsets are also contradictory. The aim of this study was to determine effects of venlafaxine versus fluoxetine on lymphocyte subsets in depressive patients. METHODS Sixty-nine patients diagnosed with major depressive disorder (MDD) according to DSM-IV and 36 healthy controls are included in the study. Sixty-nine patients were randomized to take fluoxetine (FLX) (n=33) or venlafaxine (VEN) (n=36). Serum lymphocyte subsets included CD3, CD4, CD8, CD16/56, CD19, CD45, Anti-HLA-DR which were measured by flow cytometric analyses at baseline and 6 weeks after the start of treatment. The severity of depression was evaluated with Hamilton rating scale for depression. RESULTS At baseline, patients with MDD had significantly lower CD16/56 ratio and higher CD45 ratio compared to the controls. Although numerically higher in the VEN treated patients, treatment response rates between the FLX (53%) and the VEN (75%) groups were not different statistically. CD45 values decreased significantly in the VEN group at the end of the 6 week treatment period whereas no difference was observed in the FLX group. By the 6th week, treatment responders showed a significantly higher CD16/56 ratio than non-responders. Baseline severity of depression and anxiety was positively correlated with baseline CD45 ratio and negatively correlated with baseline CD16/56 ratio. We did not observe consistent changes in the absolute number of circulating B or T cells, nor in the helper/inducer (CD4) or suppressor/cytotoxic (CD8) subsets. CONCLUSIONS CD16/56 was lower in patients with MDD and increased in treatment responders at 6th week. CD45 ratio was higher in patients with MDD than healthy subjects; it decreased with antidepressant treatment and was positively correlated with the severity of depression. Antidepressant treatment contributes to immune regulation in patients with major depressive disorder.

Determination of acute and chronic effects of cadmium on the cardiovascular system of rats

In this study, the systemic hemodynamics induced by acute and chronic cadmium (Cd+2) intoxication in the cardiovascular system of rats using thoracic electrical bioimpedance were examined and the acute and chronic effects of Cd+2 intoxication on the activities of antioxidant enzymes and malondialdehyde (MDA) were compared. Also, in this study, ultrastructural changes in the heart and aorta of rats were evaluated. Thirty-eight male Wistar albino rats were randomly divided into control, acute, and chronic groups. Chronic group was administered by oral gavage an aqueous solution of CdCl2 for 60 days, at dose of 15 mg Cd+2/kg/day. Acute group was administered by oral gavage an aqueous solution of CdCl2 with a single dose of 15 mg Cd+2/kg. Cadmium increased the stroke volume and cardiac output of rats in the chronic group, but did not change the heart rate significantly. Antioxidant enzymes activities and MDA level significantly increased in the chronic group. In ultrastructural examination, there were widespread degenerative changes in heart muscle cells of the chronic group but endothelial cells and smooth muscle cells in the aorta tissue samples had normal morphological features in all groups. All of the findings indicate that Cd+2 toxication can cause deformation in heart muscle cells due to an increase in free radicals and lipid peroxidation. Also, this study has confirmed that a long-term-Cd+2 exposure increased stroke volume (SV) and cardiac output (CO), but did not change the heart rate (HR).