It is known that the combined use of antibiotics, such as isoniazid and rifampicin, in the treatment of tuberculosis causes oxidative kidney damage. The aim of this study was to biochemically and histopathologically investigate the effect of lycopene on oxidative kidney damage due to the administration of isoniazid and rifampicin in albino Wistar male rats. Lycopene at a dose of 5 mg/kg was orally administered to lycopene+isoniazid+rifampicin (LIR) rats, and normal sunflower oil (0.5 mL) was orally administered to isoniazid+rifampicin (IR) and healthy control (HG) rats as vehicle by gavage. One hour after the administration of lycopene and vehicle, 50 mg/kg isoniazid and rifampicin were given orally to the LIR and IR groups. This procedure was performed once a day for 28 days. Rats were sacrificed by a high dose of anesthesia at the end of this period, and oxidant-antioxidant parameters were measured in the removed kidney tissues. Creatinine and blood urea nitrogen (BUN) levels were measured in blood samples, and kidney tissues were also evaluated histopathologically. The combined administration of isoniazid and rifampicin changed the oxidant-antioxidant balance in favor of oxidants, and it increased blood urea nitrogen and creatinine levels, which are indicators of kidney function. Co-administration of isoniazid and rifampicin also caused oxidative kidney damage. Lycopene biochemically and histopathologically decreased oxidative kidney damage induced by isoniazid and rifampicin administration. These results suggested that lycopene may be beneficial in the treatment of nephrotoxicity due to isoniazid and rifampicin administration.

Bevacizumab-induced vascular endothelial growth factor (VEGF) inhibition may lead to a decrease in adenosine triphosphate (ATP) levels, an increase in intracellular Na+ and Ca2+ concentrations and an increase in reactive oxygen species (ROS) generation, as well as to cell damage. To investigate the biochemical and histopathological effects of ATP, benidipine and ATP in combination with benidipine on bevacizumab-induced kidney damage in rats. Rats were divided into 5 treatment groups: bevacizumab (BVZ) alone, ATP + bevacizumab (ABVZ), benidipine + bevacizumab (BBVZ), ATP + benidipine + bevacizumab (ABBVZ), and healthy controls (HC). Adenosine triphosphate (25 mg/kg), benidipine (4 mg/kg orally), ATP (25 mg/kg) + benidipine (4 mg/kg), or saline were administered to albino Wistar rats. One hour after treatment, bevacizumab was injected at a dose of 10 mg/kg to induce kidney damage. Two doses of bevacizumab were delivered 15 days apart. Adenosine triphosphate + benidipine were administered once a day for 1 month. Malondialdehyde (MDA), total oxidant status (TOS), creatinine, and blood urea nitrogen (BUN) levels of the BVZ, BBVZ, ABVZ, ABBVZ, and HC groups were ranked from highest to lowest. Conversely, total glutathione (tGSH) and total antioxidant status (TAS) kidney tissue values were ranked from lowest to highest, respectively. Hemorrhage, tubular necrosis and grade 3 focal tubular atrophy were observed in the BVZ group. Atrophy and grade 2 necrosis were observed in the BBVZ group and atrophy and grade 1 necrosis were observed in the ABVZ group. Only grade 1 atrophy was observed in the ABBVZ group. Adenosine triphosphate reduced bevacizumab-induced renal toxicity significantly more effectively than benidipine. However, the combination of ATP + benidipine further reduced bevacizumab-induced renal toxicity relative to benidipine or ATP alone. These data indicate that ATP + benidipine might be a potential therapeutic strategy for the prevention of bevacizumab-induced renal toxicity.

Objective: To evaluate outcomes of concurrent inguinal hernia (IH) repair with mesh during transperitoneal robot-assisted radical prostatectomy (RARP). Material and Methods: Data of 26 patients (31 procedures) undergoing IH repair concurrently with RARP between January 2017 and January 2020 were evaluated retrospectively. Patients’ demographics, intraoperative and postoperative variables were recorded. Patients were assessed based on prostate-specific antigen recurrence, IH recurrence, mesh infection, seroma formation and groin pain quarterly in the first year, and every six month thereafter. Results: The median age was 64.5 years in our population. IH was detected preoperatively in 46.2% of patients (n = 12) and intraoperatively in 53.8% (n = 14). Twenty-one (80.8%) patients (11 of them had right IH and 10 of them had left IH) had unilateral hernias and 5 patients (19.2%) had bilateral hernias. Twenty-three (88.4%) IHs were direct, three (11.6%) were indirect. The median operative time and estimated blood loss were 192.5 (range: 140– 250) min and 100 (range: 10– 170) mL, respectively. The median duration of IH repair, time of drainage, length of hospitalization, and catheterization were 32.5 (range: 14– 40) min. 2 (range: 2– 6) days, 6 (range: 5– 8) days and 7 (range: 5– 7) days, respectively. No perioperative complication due to RARP or IH repair was observed. During a median follow-up time was 18 months, no scrotal hematoma, seroma formation or mesh infection was identified. Conclusion: IH repair performed during the same session at RARP is a safe and applicable procedure.

To examine serum paraoxonase 1 and 3 (PON1 and PON 3) activities in benign and malignant diseases of the prostate, to determine lipid profile and malondialdehyde (MDA) levels, and to investigate changes in levels following robotic-assisted laparoscopic radical prostatectomy (RALRP). 137 patients, including a control group, were enrolled in the study. These were assigned into four groups. Group 1 (n=33) consisted of previously undergoing RALRP with no recurrence, Group 2 (n=36) of patients diagnosed with prostate cancer (PCa) and undergoing RALRP, and Group 3 (n=34) of patients diagnosed with benign prostatic hyperplasia. The control group (n=34) consisted of healthy individuals. Serum Low-Density Lipoprotein (LDL), High-Density Lipoprotein (HDL), triglyceride, cholesterol, prostate-specific antigen (PSA), PON1, PON3, and MDA values were measured. In addition, Group 2 MDA, PON1, PON3, and PON1/HDL levels were investigated preoperatively and at the first month postoperatively. Significant changes were determined in PON1, PON3 and MDA levels. PON1 and PON3 levels decreased significantly in patients with PCa, while MDA levels increased. PON1 and PON3 increased postoperatively in the PCa group, while MDA decreased. BPH group PON1, PON3 and MDA levels were higher than those of the control group. An increase in free oxygen radicals in the body or a decrease in endogenous antioxidant enzyme levels can result in malignant and benign diseases of the prostate. Surgical excision of malignant tissue in PCa causes a decrease in oxidative stress.