These data suggest that SSRIs have a negative effect on testicular tissues. This negative impact is markedly greater in the paroxetine group. To determine the exact mechanism of action of these drugs on testicular tissue, well-designed randomized controlled clinical studies are needed on a larger population.

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.

Inflammatory markers are elevated in acute coronary syndromes, and are also known to play a crucial role in the pathogenesis of neointimal proliferation and stent restenosis. Drug-eluting stents (DESs) have been shown to decrease stent restenosis in different studies. In this study, we aimed to investigate the effect of treatment with DESs on systemic inflammatory response in patients with unstable angina pectoris who underwent percutaneous coronary intervention (PCI). We compared plasma high-sensitivity C-reactive protein (hsCRP), human tumor necrosis factor alpha (Hu TNF-alpha), and interleukin 6 (IL-6) levels after DES (dexamethasone-eluting stent [DEXES], and sirolimuseluting stent [SES]) implantation with levels after bare metal stent (BMS) implantation. We performed PCI with a single stent in 90 patients (62 men; 59 +/- 9 years of age; n = 30 in the BMS group, n = 30 in the DEXES group, n = 30 in the SES group) who had acute coronary syndrome. Plasma hsCRP, Hu TNF-alpha, and IL-6 levels were determined before intervention and at 24 h, 48 h, and 1 week after PCI. The results were as follows. Plasma hsCRP levels at 48 h (11.19 +/- 4.54, 6.43 +/- 1.63 vs 6.23 +/- 2.69 mg/l, P = 0.001) after stent implantation were significantly higher in the BMS group than in the DES group; this effect persisted for 7 days (P = 0.001). Plasma Hu TNF-alpha levels at each time point were higher in the SES group than in the BMS and DEXES groups (P < 0.05). The time course of Hu TNF-alpha values was similar in all groups. Although IL-6 levels at baseline and at 24 and 48 h showed no statistically significant difference between the study groups, postprocedural values at 7 days were slightly statistically significant in the SES group (P = 0.045). Drug-eluting stents showed significantly lower plasma hsCRP levels after PCI compared with BMSs. This may reflect the potent effects of DESs on acute inflammatory reactions induced by PCI.

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.

This study aimed to investigate the protective effect of sinapic acid (SA) on biochemical and histopathological changes in an experimental testicular torsion‐detorsion rat model. Twenty‐four rats were randomised into four groups: sham group, ischemia/reperfusion (IR) group subjected to testicular torsion for 2 hr and then detorsion for 4 hr, and two groups treated with SA1 and SA2 (10 mg/kg and 20 mg/kg, by single intraperitoneal injection, 30 min before reperfusion). Serum testosterone, follicle‐stimulating hormone (FSH), and luteinizing hormone (LH) were measured by an autoanalyzer, superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), malondialdehyde (MDA), protein carbonyl (PC), and nitric oxide (NO) oxidative stress parameters by spectrophotometric methods, and tumour necrosis factor (TNF‐α), interleukin‐1 beta (IL‐1β), and interleukin 6 (IL‐6) parameters by the Elisa method. In addition, immunohistochemical and histopathological examinations were performed on testicular tissues. There was no significant difference between the groups in terms of serum testosterone, FSH and LH levels (p > .05). SA significantly reduced increased testicular damage, oxidative stress, inflammation, cell death and also restored decreased antioxidant enzyme activities (p < .05). Pre‐treatment of rats with SA reduced testicular dysfunction and morphological changes IRI. SA's antioxidant, anti‐inflammatory, and antiapoptotic properties were found to be protective against testicular IR.