Browsing by Author "Oksuz, Ersoy"

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Comparison of Effects of High and Low Dose Paracetamol Treatment and Toxicity on Brain and Liver in Rats
(Kare Publ, 2020) Oksuz, Ersoy; Yasar, Semih; Erten, Remzi; Arihan, Okan; Oto, Gokhan
OBJECTIVE: Paracetamol is thought that it acts by inhibiting the central cyclooxygenase (COX) enzyme; its mechanism of action is still not fully explained. Although its most important side effect is hepatoxicity, it is thought to cause toxicity on the brain in recent years. The present study aims to investigate the treatment and toxic effects of low and high doses of paracetamol on the liver and brain. METHODS: Wistar-albino rats were used in this study. At doses of 20-500 mg/kg, paracetamol was administered intraperitoneally once a day for one and three days. The brain and liver were used for immunohistochemical evaluation using COX-3, prostaglandin E-2 (PGE(2)) and caspase 3 antibodies and for total antioxidant (TAS), total oxidant ( TOS) and oxidative stress index (OSI) measurements. Results were evaluated using the Kruskal Wallis test (SPSS ver.24). RESULTS: The liver COX-3 levels were significantly lower in both groups with higher doses (p<0.05). In the brain, there was no statistically significant difference in COX-3 levels between the groups. There was no statistically significant difference in PGE(2) levels in the liver and brain between the groups (p>0.05). The caspase 3 level in the liver was statistically significantly higher in the low dose group compared to the other groups (p<0.05). In both liver and brain, OSI values were significantly higher in the 3-day high-dose group compared to others (p<0.05). There was no statistically significant difference between the groups in ALT and AST values (p>0.05). CONCLUSION: The results of our study show that paracetamol inhibits the COX-3 enzyme in the liver but has no effect in the brain, and COX-3 does not have an effect on PGE(2). Paracetamol causes apoptosis in the liver only in low doses; higher doses may cause toxicity by increasing oxidative stress, especially in the brain.
Effect of Paracetamol in the Proliferation of Glioblastoma Cell Line: the Role of Apoptosis, Cox-2 and Cyclin B Expressions
(Turkish Neurosurgical Soc, 2021) Oksuz, Ersoy; Gorgisen, Gokhan; Ozdemir, Hulya; Gulacar, Ismail Musab; Oto, Gokhan
AIM: To investigate the relationship between paracetamol and expression levels of cyciooxygenase-2, cyclin B, cell viability and apoptosis in glioblastoma cell line. MATERIAL and METHODS: The A172 glioblastoma cells were treated with different concentrations of paracetamol and phosphate buffer saline as a vehicle for 24, 48, and 72 hours. Cell viability was detected by MTT. Bax, procaspase 3, COX-2 and Cyclin B expressions were detected using Western blotting. RESULTS: A paracetamol treatment of 0.5 mg/mL for 24, 48, and 72 hours led to a 14%, 31%, and 37% decrease in cell viability. The expression of COX-2 and cyclin B levels decreased by 36% and 52% respectively, after treatment with 0.5 mg/mL paracetamol. Treatment with 0.5 mg/mL and 1 mg/mL paracetamol significantly induced the expression of cleaved caspase 3, procaspase 3 and Bax proteins compared to the control group (60%, 40%, 21%, %100, 18%, 17%, respectively). CONCLUSION: The results of our study showed that paracetamol has antitumoral effects on glioblastoma cells and this activity was induced by different signaling pathways.
A New Approach in the Treatment of Traumatic Brain Injury: the Effects of Levosimendan on Necrosis, Apoptosis, and Oxidative Stress
(Elsevier Science inc, 2022) Aycan, Abdurrahman; Oksuz, Ersoy; Gonullu, Edip; Kume, Tuncay; Ergur, Bekir; Akyol, Mehmet Edip; Kuyumcu, Fetullah
- OBJECTIVE: Traumatic brain injury (TBI) is an essential and common health problem worldwide. Levosimendan is an inotropic and vasodilator drug used to treat heart failure. Moreover, it exerts pleiotropic effects and, thus, protective effects on many organs. The present study aimed to investigate the effect of levosimendan on necrosis, apoptosis, and reactive oxygen species in rats with TBI. - METHODS: The study included 28 female Wistar-Albino rats weighing 200-250 g. The rats were divided into 4 groups with 7 rats each as follows: Group 1: No trauma group (Control), Group 2: Traumatized, untreated group (T), Group 3: Levosimendan was administered at a dose of 12 mg/kg intraperitoneally 1 hour after the trauma (L1), Group 4: Levosimendan was administered at a dose of 12 mg/kg intraperitoneally 2 hours after the concussion (L2). After the experiment, the rats were decapitated, and the brain tissue was removed. Necrosis was assessed with Cresyl violet staining, apoptosis was assessed with immunohistochemical analysis, superoxide dismutase and catalase levels were measured with the spectrophotometric method, and malondialdehyde (MDA) levels were assessed by High-Performance Liquid Chromatography. - RESULTS: The number of necrotic cells in the L1 and L2 groups was significantly lower than in the K and T groups (P = 0.015 and P = 0.03, respectively). Although the active caspase-3 level was signified considerably in the T, L1, and L2 groups compared to the K group, no significant difference was found among these 3 groups (P > 0.05). The results of superoxide dismutase levels were similar to those of active caspase-3. catalase level was significantly higher in the K group than in the T and L2 groups (P = 0.045). Malondialdehyde activity was considerably higher in the L1 and L2 groups compared to the K group (P = 0.023). - CONCLUSIONS: Our results indicated that levosimendan may exert a neuroprotective effect by reducing necrosis in TBI and that levosimendan does not affect apoptosis and antioxidant levels in TBI. Comprehensive studies are needed to elucidate the effect of levosimendan on TBI fully.
A New Approach in the Treatment of Traumatic Brain Injury: the Effects of Levosimendan on Necrosis, Apoptosis, and Oxidative Stress (Vol 168, Pg E432, 2022)
(Elsevier Science inc, 2023) Aycan, Abdurrahman; Oksuz, Ersoy; Gonullu, Edip; Kume, Tuncay; Ergur, Bekir; Akyol, Mehmet Edip; Kuyumcu, Fetullah
Relationship Between Mthfr Gene Polymorphisms and Gastrointestinal Tumors Development: Perspective From Eastern Part of Turkey
(Taylor & Francis inc, 2022) Oksuz, Ersoy; Gorgisen, Gokhan; Oto, Gokhan; Ozdemir, Hulya; Aras, Abbas; Oksuz, Murat; Demirkol, Muhammet Hamdi
Background Gastric and esophageal cancers are 2 of the most prevalent cancer types worldwide. Polymorphisms in the genes that code the methylenetetrahydrofolate reductase (MTHFR) enzyme increase the formation of both cancer types. In this study, it was aimed to research the relationship between the existence of MTHFR C677T and A1298C polymorphisms in patients with gastric and esophageal cancer and the lifespans of patients. Methods and Materials This prospective study was performed at Van Yuzuncu Yil University. Included in the study were 30 patients with esophageal tumors, 70 patients with gastric tumors, and 61 healthy volunteers. From each of the patients, 5 mL of blood was drawn. DNA was isolated via kits with spin-column technology. Results It was concluded that the risk of developing gastric cancer was 4.13 times higher in individuals who had the AC genotype of the A1298C polymorphism when compared to those who had the AA genotype, while the risk was 2.91 times higher in individuals who had the CC genotype when compared to those who had the AA genotype (P = 0.001, P = 0.027). Carriers of the AC genotype of the A1298C polymorphism had 2.89 times higher risk of developing esophageal cancer when compared to those who had the AA genotype (P = 0.033). It was determined that individuals who had the 1298 CC genotype were not at higher risk of developing esophageal cancer when compared to those with the AA genotype (P = 0.863). It was concluded that individuals who had the TT genotype of the C677T polymorphism were not at higher risk of developing gastric and esophageal cancers when compared to those who had the 677CC genotype (P > 0.05). There was no difference in terms of the life spans of the patients with regards to the genotypes (P > 0.05). Conclusion The results showed that the A1298C polymorphism on the MTHFR gene can be a risk factor for gastric and esophageal cancer in eastern Turkey. These polymorphisms may have no effect on the life spans of the patients.
Role of Sedative-Hypnotic Agents in Neurodegeneration: Effects of Midazolam and Thiopental on Apoptosis and Oxidative Stress Expression in Neonatal and Adult Rat Brains
(Turkish Neurosurgical Soc, 2022) Soyalp, Celaleddin; Oksuz, Ersoy; Gorgisen, Gokhan; Gulacar, Ismail Musab; Yasar, Semih; Tuncdemir, Yunus Emre; Acun Delen, Leman
AIM: To investigate the effects of midazolam (MDZ) and thiopental on neonatal and adult rat brains. MATERIAL and METHODS: The study included adult and 7-day-old rats that were administered 9 mg/kg of MDZ, 60 mg/kg of thiopental, or both. The Bax, procaspase-3, and caspase-3 levels were assessed using Western Blot analysis and the total oxidative stress index (OSI) values were measured spectrophotometrically. RESULTS: The procaspase-3 and caspase-3 levels were 12% and 6% lower in the neonatal MDZ group when compared to the control group. The Bax, procaspase-3, and caspase-3 levels were higher in the neonatal thiopental group by 25%, 4%, and 34%, and in the MDZ group by 16%, 19%, and 43% when compared to the neonatal control group. In the adult rats, the caspase-3 levels were 10 times higher in the MDZ group when compared to the control and thiopental groups. Moreover, the caspase-3 levels were 7 times higher in the adult thiopental group when compared to the control group. The OSI values in the neonatal rats were significantly higher in the neonatal MDZ and neonatal thiopental groups when compared to the control group (p<0.05). Similarly, the OSI values in the adult rats were significantly higher in the neonatal MDZ and neonatal thiopental groups when compared to the control group CONCLUSION: MDZ and thiopental may promote apoptosis and oxidative stress, and thereby result in neurotoxicity, with MDZ showing a greater effect in adults and thiopental showing a greater effect in neonates.
Serum Total Sialic Acid and Lipid-Linked Sialic Acid May Be the New Potential Biomarkers in Paracetamol Nephrotoxicity
(Aves, 2020) Oksuz, Ersoy; Bugday, Muhammet Serdar; Demir, Feyza; Ekin, Suat; Arihan, Okan; Oto, Gokhan
Objective: In recent years, paracetamol has been shown to have toxic effects on the kidneys. Sialic acid (SA), an important component of the cell membranes, increases in many pathological conditions. This study aimed to investigate the effects of different doses of paracetamol on the kidney tissue and serum total SA (TSA) and lipid-bound SA (LSA) levels. Materials and Methods: A total of 5 different groups were formed, with 8 rats in each group; 20 and 500 mg/kg/intraperitoneal paracetamol was applied to the groups once daily for 1 and 3 days, respectively. Renal pathology was evaluated with hematoxylin and eosin. TSA/LSA levels and urea/creatinine levels were measured from the blood samples taken from the rats. Results: TSA levels were significantly higher in the groups in which paracetamol was administered in a single dose and 500 mg/kg dose for 3 days than control (p<0.05 and p<0.001). LSA levels were significantly higher in the groups that received 1 and 3 doses of 500 mg/kg/day and 3 doses of 20 mg/kg than control (p<0.05, p<0.001, and p<0.05). Conclusion: SA levels may be a specific marker for kidney damage because of the increase in the SA levels in direct proportion to this level of renal degeneration.