The effects of trimetazidine and sildenafil on bilateral cavernosal nerve injury induced oxidative damage and cavernosal fibrosis in rats.

AIM: The aim of this study was to compare the effects of sildenafil and trimetazidine on bilateral cavernosal nerve injury-induced oxidative damage and fibrotic changes in cavernosal tissue in rat model. MATERIAL AND METHODS: A total of 32 male Sprague-Dawley rats were randomly divided into 4 groups; each group consist 8 rats (control, BCI, BCI + TMZ, and BCI + sildenafil groups). Tissue superoxide dismutase (SOD), malondialdehyde (MDA), and protein carbonyl (PC) levels were determined biochemically and distribution of cavernosal fibrosis density among groups was performed histopathologically. RESULTS: Tissue SOD levels in BCI group were significantly lower than the control group (P < 0.05). Tissue MDA and PC levels in BCI group were significantly higher than the control group (P < 0.05). TMZ and sildenafil administration significantly increased tissue SOD levels (P < 0.05) and reduced tissue MDA and PC levels (P < 0.05). Histologically, the degree of cavernosal fibrosis and collagen density was higher in BCI group in comparison to control, TMZ-treated, and sildenafil-treated groups. CONCLUSION: BCI caused oxidative damage and increased cavernosal fibrosis in rat penis. TMZ and sildenafil treatment decreased oxidative damage and reduced the degree of fibrosis in penile tissue due to BCI.

The effect of carvedilol on serum and tissue oxidative stress parameters in partial ureteral obstruction induced rat model.

Although the pathological mechanism underlying kidney damage is not completely understood, it has been reported that reactive oxygen species (ROS) formed during ureteral obstruction may play an important role in this process. Carvedilol has been used in a limited number of studies examining oxidative injury. The aim of this study was to investigate the effect of carvedilol on serum and tissue oxidative stress parameters in the partial unilateral ureteral obstruction (PUUO)-induced rat model. To our knowledge, the protective effects of carvedilol in the PUUO-induced rat model have not been reported. Twenty-six male Wistar albino rats, age 5.5 to 6 months and weighing 250 to 300 g, were used in this study. The rats were randomly divided into three groups. In Group 1 (n = 9), the control group, a sham operation was performed. In Group 2 (n = 8), the PUUO group, the left ureter was embedded into the psoas muscle to create PUUO and maintained for 7 days. In Group 3 (n = 9), carvedilol was orally administered to the rats (2 mg/kg). After the establishment of PUUO, carvedilol was given for the following 7 days. After partial unilateral ureteral obstruction, a nephrectomy was performed to determine the blood and tissue levels of superoxide dismutase (SOD), malondialdehyde (MDA), protein carbonyl (PC), and nitric oxide (NO). The median SOD, MDA, PC, and NO levels in the tissues were 0.006 U/mg protein, 5.11 nmol/g protein, 4.31 nmol/mg protein, and 0.337 µmol/g protein in the control group, respectively. There was a significant increase in tissue SOD (p = 0.014), MDA (p = 0.002), and NO (p = 0.004) levels in Group 2. However, a statistically significant difference was not observed in PC (p = 0.847) enzymatic activity in Group 2. When compared with Group 2, carvedilol treatment caused a reduction in NO (p = 0.003), and PC (p = 0.001) activities in Group 3. The serum SOD (p = 0.004), MDA (p = 0.043), PC (p = 0.043), and NO (p = 0.001) levels were significantly different in Group 3 compared with Group 2. Administration of carvedilol also reduced the detrimental histopathologic effects caused by PUUO. According to histopathological examination of the renal tissues, the inflammation rates were 22.2%, 87.5% and 33.3% in Groups 1, 2, and 3, respectively (p < 0.05). The results of the present study show that partial unilateral ureteral obstruction caused oxidative stress in the serum and kidney tissues of rats, and treatment with carvedilol reduced the harmful effects of ureteral obstruction.

Effects of melatonin on partial unilateral ureteral obstruction induced oxidative injury in rat kidney.

AIM: This experimental study was designed to produce ischemia-reperfusion injury in rat kidney by performing partial unilateral ureteral obstruction (PUUO) and investigated the effects of melatonin on the levels of oxidative injury parameters. MATERIALS AND METHODS: Twenty-four adult male rats were randomly divided into three groups as follows; control group (Group 1); only nephrectomy and blood (5 ml) drawn from vena cava inferior, PUUO group (Group 2); PUUO (10 days)+ipsilateral nephrectomy after recovery of PUUO+blood from vena cava inferior VCI, melatonin treated group (Group 3); PUUO (10 days)+melatonin (1/2 hr before release, 50 mg/kg, ip)+ipsilateral nephrectomy after recovery of PUUO+blood from VCI. The left ureter was embedded into the psoas muscle to create PUUO. After 10 days, PUUO was recovered and ipsilateral nephrectomies were performed for biochemical analysis of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and protein carbonyl (PC) in the tissues and blood was drawn from inferior vena cava to study the same parameters in systemic circulation. The results were compared statistically. RESULTS: The blood levels of MDA, NO, and PC were increased in the PUUO group in comparison to the sham-operated group (P<0.05). Melatonin treatment reduced MDA, NO, and PC levels in blood after PUUO recovery, but statistically significance consisted only for MDA and NO (P<0.05). The antioxidant enzyme activities (SOD, GSH-Px) were increased in the PUUO group (P<0.05). Melatonin treatment reduced SOD and GSH-Px activities in comparison with the sham-operated control group (P<0.05). Similarly, renal tissue levels of MDA, NO, and PC were increased in the PUUO group in comparison with the sham-operated group (P<0.05). Melatonin treatment ameliorated MDA, NO, and PC levels in renal tissue after PUUO recovery only MDA was statistically significant (P<0.05). Antioxidant enzyme activities (SOD, CAT, and GSH-Px) were increased in the PUUO group. Melatonin treatment caused reduction in SOD, CAT, and GSH-Px activities in comparison to the sham-operated control group (P<0.05). CONCLUSION: The results of this study showed that experimentally induced PUUO caused oxidative stress in rat kidney and melatonin treatment reduced oxidative stress and therefore may have a preventive effect on PUUO induced oxidative kidney damage in rats.

Oxidative status in the lungs associated with tobacco smoke exposure.

BACKGROUND: Oxidative stress has a critical role in inflammatory responce against tobacco smoke (TS). Testing exhaled breath condensate (EBC) samples is one of the methods used for assessment of airway inflammation caused by TS. We aimed to investigate oxidative stress in the lungs associated with TS and to evaluate the effect of this stress with pulmonary function tests (PFTs). METHODS: We included 69 subjects as three groups into the study (Group I; 26 smokers, Group II; 21 passive smokers, Group III; 22 non-smokers without TS exposure). Levels of malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), nitrite/nitrate [index of nitric oxide (NO) production], vitamin C, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were measured in EBC samples collected using a condenser and PFTs were performed. RESULTS: The levels of MDA, 8-OHdG, SOD and GSH-Px were higher in smokers. NO levels gradually increased from Group I to Group III. MDA levels were lower in Group III than Group II. The levels of vitamin C were similar in all groups. We determined negative correlation between 8-OHdG levels and forced expiratory volume in one second (FEV1), and maximum mean expiratory flow (MMEF), and a positive correlation between SOD levels and FEV1. CONCLUSIONS: TS exposure affected the balance between oxidative stress and antioxidant capacity of lungs. Preventing environmental TS exposure might decrease oxidative damage. Increased levels of 8-OHdG and SOD levels could be assessed as an early sign of airway damage.