The effects of thiopental on cold ischemic injury in renal transplantation.

INTRODUCTION: One of the most important factors influencing post-transplant success in kidney transplantation is preserving the viability of the organ from removal to transfer into the recipient. AIM: This study aimed to reduce the energy requirement with thiopental doses administered before organ transplantation, and to increase the organ viability by minimizing the tissue damage during the cold ischemia process. MATERIALS AND METHODS: Twenty female Wistar albino rats were divided into two groups: control group (group C), and thiopental group (group T). In group C, a midline incision was performed, and the renal artery was isolated under ketamine and xylazine anesthesia. A standard organ storage solution (cooled to +4°C) was used for kidney perfusion. Nephrectomy was applied, and the removed kidneys were placed into +4°C standard organ storage solution and stored at +4°C for 12 hours. Animals in group T were subjected to the procedures explained above under 85 mg/kg thiopental sodium anesthesia. After 12-hour storage, samples from the kidney tissues were fixed in 10% neutral buffered formalin. Histopathological evaluation and apoptosis detection via TUNEL method were performed. RESULTS: Tubular necrosis was more extensive in group C compared with that in group T and this difference was statistically significant. Similarly, vacuolization was widely observed in group C, and this increase was also statistically significant. For the 'dilatation of Bowman's space' parameter, a significant decrease was observed in group T compared with group C. When the apoptotic index values of both groups were examined, it was seen that they were lower in group T than those in group C. This result was statistically significant. CONCLUSIONS: These data suggest that thiopental provides protection to the kidney tissue during the cold storage process. Thiopental has been shown to decrease the number of apoptotic cells in the kidney tissue when administered to the donor before organ transplantation, increasing the organ viability.

Effects of Ozone Therapy on Chronic Arsenic Poisoning in Rats.

Arsenic (As) is a toxic metalloid that affects many organs through drinking water. This study aims to examine the efficacy of ozone therapy on chronic arsenic toxicity. Twenty-four male Wistar albino rats were housed in individual cages and grouped as control, As, O3, and As + O3. As was applied by adding 5 mg/kg/day in drinking water for 60 days. Ozone therapy was applied at 0.5 mg/kg/day (i.p.) O3 in the last 5 days of the experimental period. Tissues were harvested and analyzed for histopathological injury and apoptotic markers. There was no significant difference between the As + O3 and O3 groups (p = 0.186 and p = 0.599) for light microscopic criteria: inflammatory cell infiltration and hydropic degeneration in liver tissue.In TUNEL assessments, similar outcomes were obtained in the control and As + O3 groups. A statistically significant increase was observed in p53 and Caspase 3 (Casp-3) expression levels in the As group compared to the O3 and As + O3 groups. There was no significant difference between the As + O3 and O3 groups on peritubular hemorrhage and desquamation parameters in kidneys (p = 0.147 and p = 0.094). The KIM-1 expression level was significantly increased in the As group compared to the As + O3 group (p = 0.01), and the Casp-3 expression level was not significantly changed in the O3 group compared to the As + O3 group (p = 0.59). In conclusion, it is determined that ozone therapy has ameliorative effects on the microscopic injury of liver and kidney tissues. In addition to microscopic improvement, KIM-1 gene expression levels were ameliorated in the kidneys. The apoptotic cell counts and the Casp-3 and p53 gene expression levels were decreased by O3 administration. Thus, ozone therapy can be a treatment choice for As toxicity.

Effects of hyperbaric oxygen treatment on liver and kidney tissue in chronic arsenic toxicity.

Arsenic (As) is a toxic substance that damages the human body through exposure to drinking water. This exposure damages many organs and tissues in the body, especially the liver and kidneys. Hyperbaric oxygen (HBO2) therapy is a treatment method that acts by reducing oxidative stress parameters in tissues with high-pressure oxygen. Based on this, our study aimed to investigate the effectiveness of HBO2 on liver and kidney tissues with chronic arsenic toxicity. In the study 24 male Wistar albino rats (220-300 g, two to three months old) were equally divided into four groups: Control; As; HBO2; and As+HBO2. All animals were housed in individual cages. The toxicity model was created by adding arsenic to drinking water at a dose of 5 mg/kg/day for 60 days. HBO2 was applied 2 ATA pressure for 90 minutes a day for five days. At the end of the study, liver and kidney tissues were taken and stored for analysis. In liver tissue, histopathological showed that arsenic reduced inflammatory cell infiltration, sinusoidal congestion, and hydropic degeneration, while HBO2 increased these measures. Similar results were found by TUNEL method. In kidney tissue, both histopathologic and TUNEL method examinations found similar results with the liver: The As group was more damaged than the As+HBO2 group.

The Effect of Topically Applied Boric Acid on Ephrin-Eph Pathway in Wound Treatment: An Experimental Study.

Background: Wound healing has a vital importance for the organism and various agents are used to accelerate wound healing. Although the effect of boron on wound healing is known, its mechanisms are not completely clear yet. In this study, the effect of boron in the Ephrin /Eph pathway will be evaluated. Methods: Forty adult female rats were used in the study. A full-thickness excisional wound model was created in all groups divided as Control, Fito, Boron and Plu groups. After the applications performed twice a day and lasting 7 days, skin tissues obtained and evaluated histopathological (inflammatory cell infiltration, oedema, and fibroblast proliferation density) and immunohistochemical (TNF-α, EphrinA1, EphrinB1, EphrinB2 and EphB4). Results: Inflammatory cell infiltration score was found to be higher in the Fito group compared to Boron group (p = .018). Fibroblast proliferation density was higher in Plu group than Boron group (p = .012). While TNF-α was lower in boron group than Plu (p = .027) and Fito (p = .016) groups, EphrinA1 was higher in Boron group than Plu group (p = .005). EphrinB1 expression was higher in Boron group compared to Plu (p = .015) and Fito (p = .015) groups, and the same difference was also observed in EphrinB2 (p values .000). Similarly, EphB4 immunoreactivity was higher in the Boron group compared to Plu (p = .000) and Fito (p = .002). Conclusion: One of the mechanisms of action of boron in wound healing is to increase EphrinB1, EphrinB2 and EphB4. Low TNF-α and histopathological findings indicate that boron limits extensive wound healing.