Testicular torsion (T)/detorsion (D) can cause testicular injury due to the rotation of the spermatic cord and its vessels, therefore it represents an urological emergency that is surgically treated. Oxidative damage occurs in the testis and distant organs because of the overproduction of free radicals and overexpression of proinflammatory cytokines by reperfusion after surgery. Cerium oxide (CeO₂) nanoparticles, a material also known as nanoceria, have regenerative antioxidant properties on oxidative stress. The present study aimed to investigate the effects of nanoceria on testis tissues in testicular T/D in rats. A total of 24 rats were equally and randomly divided into four groups: Control, CeO₂, T/D and CeO₂‑T/D groups. Left inguinoscrotal incision was performed in the control group. In the CeO₂ group, 0.5 mg/kg CeO₂ was given intraperitoneally 30 min before inguinoscrotal incision. In the T/D group, unilateral testicular T/D was performed through an inguinoscrotal incision and rotating the left testis 720˚ clockwise, which was then left ischemic for 120 min, followed by 120 min of reperfusion. In the CeO₂‑T/D group, 0.5 mg/kg CeO₂ was given intraperitoneally 30 min before testicular T/D. At the end of the experiment, testis tissues were removed for histopathological and biochemical examinations. The samples were histologically examined, Glutathione‑s transferase (GST), catalase (CAT), paraoxonase (PON) activities and malondialdehyde (MDA) levels were measured via biochemical analysis methods, while the expression levels of p53, Bax and Bcl‑2 were detected using immunohistochemistry. The present results revealed statistically significant inter‑group differences in PON, CAT and GST activities and MDA levels. GST, CAT and PON activities were significantly higher, whereas MDA levels in the CeO₂‑T/D group were significantly lower compared with those in the T/D group. The T/D group had increased Bax and decreased Bcl‑2 expression levels in their seminiferous tubules compared with the control and CeO₂ groups. CeO₂ treatment led to downregulation of Bax and upregulation of Bcl‑2. The expression of p53 was high in the T/D group compared with that in the control and CeO₂ groups, and was upregulated in all germinal cells. However, compared with that in the T/D group, p53 expression was significantly decreased in the CeO₂‑T/D group. The testicular injury score significantly increased in the CeO₂‑T/D group compared with the control and CeO₂ groups. Rats in the CeO₂‑T/D group demonstrated significantly milder tissue lesions compared with those in T/D group. The present findings indicated that nanoceria may protect testis in rats against the harmful effects of T/D. Further studies are required to evaluate how CeO₂ reduces oxidative stress and cell death in testis tissue that underwent T/D‑related injury.

Diabetic complications and lipid peroxidation are known to have a close association. Lipid peroxidation commonly occurs at sites exposed to ischaemia, but distant organs and tissues also get damaged during ischaemia/reperfusion (I/R). Some of these targets are vital organs, such as the lung, liver, and kidney; the lung is the most frequently affected. The aim of our study was to investigate the effects of dexmedetomidine on I/R damage in lung tissue and on the oxidant/anti-oxidant system in diabetic rats. Diabetes was induced with streptozotocin (55 mg/kg) in 18 Wistar Albino rats, which were then randomly divided into three groups (diabetes control (DC), diabetes plus ischaemia-reperfusion (DIR), and diabetes plus dexmedetomidine-ischaemia/reperfusion (DIRD)) after the effects of diabetes were clearly evident. The rats underwent a left thoracotomy and then ischaemia was produced in the myocardium muscle by a left anterior descending artery ligation for 30 min in the DIR and DIRD groups. I/R was performed for 120 min. The DIRD group received a single intraperitoneal dose of dexmedetomidine (100 µg/kg); the DIR group received no dexmedetomidine. Group DC was evaluated as the diabetic control group and also included six rats (C group) in which diabetes was not induced. These mice underwent only left thoracotomy and were closed without undergoing myocardial ischaemia. Histopathological changes, activities of catalase (CAT) and glutathione-S-transferase anti-oxidant enzymes, and malondialdehyde (MDA) levels were evaluated in the lung tissues of all rats. Neutrophil infiltration/aggregation was higher in the DIR group than in the C, DC, and DIRD groups (p=0.001, p=0.013, and p=0.042, respectively). The lung injury score was significantly higher in the DIR group than in the C and DC groups (p<0.0001 and p=0.024, respectively). The levels of MDA were significantly higher in the DIR group than in the C and DIRD groups. CAT activity was significantly higher in the DIR group than in the DIRD and C groups. Our results confirm that dexmedetomidine has protective effects against the lung damage resulting from I/R in diabetic rats. Future studies conducted to evaluate the effects of the use of dexmedetomidine on damage to various organs following different I/R durations may help understanding possible protective effects of dexmedetomidine and underlying mechanisms in tissue damage related to I/R injury.

Background: Ischaemia–reperfusion (IR) injury, which can be encountered during surgical procedures involving the abdominal aorta, is a complex process that affects distant organs, such as the heart, liver, kidney, and lungs, as well as the lower extremities. In this study, we aimed to contribute to the limited literature by investigating the protective effect of dexmedetomidine, which was administered through different routes, on kidney tissue in rats with spinal cord IR injury. Methods: A total of 30 rats were randomly divided into five groups: control (C group), IR (IR group), IR-intraperitoneal dexmedetomidine (IRIPD group), IR-intrathecal dexmedetomidine (IRITD group), and IR-intravenous dexmedetomidine (IRIVD group). The spinal cord IR model was established. Dexmedetomidine was administered at doses of 100 μg/kg intraperitoneally, 3 μg/kg intrathecally, and 9 μg/kg intravenously. Histopathologic parameters in kidney tissue samples taken at the end of the reperfusion period and biochemical parameters in serum were evaluated. Results: When examined histopathologically, tubular dilatation was found to be significantly reduced in the IRIVD, IRITD, and IRIPD groups compared with the IR group (p = 0.012, all). Vascular vacuolization and hypertrophy were significantly decreased in the IRIVD, IRITD, and IRIPD groups compared with the IR group (p = 0.006, all). Tubular cell degeneration and necrosis were significantly reduced in the IRIVD, IRITD, and IRIPD groups compared with the IR group (p = 0.008, p = 0.08, and p = 0.030, respectively). Lymphocyte infiltration was significantly decreased in the IRIVD and IRITD groups compared with the IR group (p = 0.006 and p = 0.06, respectively). Conclusion: It was observed that dexmedetomidine administered by different routes improved the damage caused by IR in kidney histopathology. We think that the renoprotective effects of dexmedetomidine administered intravenously and intrathecally before IR in rats are greater.

Dexmedetomidine protects against lipid peroxidation and erythrocyte deformability alterations in experimental hepatic ischemia reperfusion injury

Introduction: Oxidative stress has an important role in the pathophysiology of Alzheimer’s disease (AD), the most common type of dementia. Boric acid (BA) contributes significantly to the protection of the brain by reducing lipid peroxidation and supporting antioxidant defense. We aimed to evaluate the therapeutic potential of BA treatment in AD rats. Materials and Methods: Four groups were formed as Control (C), Alzheimer’s (A), Alzheimer’s + Boric acid (ABA), Boric acid (BA). Intracerebroventricular injection of Streptozotocin (STZ) was preferred to create an AD. After 4 weeks, BA was applied 3 times every other day. The Radial Arm Maze Test (RAMT) was used to evaluate memory and learning abilities. Biochemical and histopathological evaluations were made in the hippocampus. Results: Initial RAMT inlet/outlet (I/O) numbers were similar. Two weeks after STZ injection, I/O numbers decreased in group A and ABA compared to group C and BA (p< 0.05). After the second BA application, I/O numbers increased in the ABA group compared to the A group (p< 0.05). In group A, PON-1, TOS and OSI levels were higher and TAS levels were lower than in groups BA and C. After BA treatment, PON-1 and OSI levels were lower in the ABA group than in the A group (p< 0.05). Although there was an increase in TAS value and a decrease in TOS, this did not make a statistical difference. The thickness of the pyramidal cell in CA1 and the granular cell layers in the dentate gyrus, and the number of intact and degenerated neurons in the pyramidal cell layer were similar between the groups. Discussion: Significant improvement in learning and memory abilities after BA application is promising for AD. Conclusion: These results show that BA application positively affects learning and memory abilities, and reduces oxidative stress. More extensive studies are required to evaluate histopathological efficacy.