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Öğe Amelioration of oxidative damage parameters by carvacrol on methanol-induced liver injury in rats(Int Press Editing Centre Inc, 2022) Gursul, Cebrail; Ozcicek, Adalet; Ozkaraca, Mustafa; Mendil, Ali Sefa; Coban, Taha Abdulkadir; Arslan, Aynur; Ozcicek, FatihThe methanol metabolite that causes hepatotoxicity is formic acid, generating reactive oxygen radical formation and cell damage. Carvacrol is an antioxidant monoterpenic phenol produced from Thymus vulgaris. This study aimed to investigate the effects of carvacrol on methanol-induced oxidative liver damage in rats. Eighteen rats were divided into three groups. Methotrexate was administered orally for 7 days to methotrexate+methanol (MTM) and methotrexate+methanol+carvacrol (MMC) groups. Methotrexate was given before methanol to cause methanol poisoning. Distilled water was given to the healthy group (HG) as a solvent. At the end of the 7th day, 20% methanol was administered orally at a dose of 3 g/kg to the MTM and MMC groups. Four hours after methanol administration, 50 mg/kg carvacrol was injected intraperitoneally into the MMC group. Animals were sacrificed 8 h after carvacrol injection. Biochemical markers were studied in the excised liver tissue and blood serum samples, and histopathological evaluations were made. Severe hemorrhage, hydropic degeneration, pycnosis, and mononuclear cell infiltration were observed in the liver of the MTM group. Additionally, the levels of malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly higher, and total glutathione (tGSH) and total antioxidant status (TAS) were significantly lower in the MTM group compared to HG (P<0.001). Carvacrol prevented the increase in MDA, TOS, ALT and AST levels with methanol and the decrease in tGSH and TAS levels (P<0.001), and alleviated the histopathological damage. Carvacrol may be useful in the treatment of methanol-induced liver damage.Öğe Apoptosis is induced by sub-acute exposure to 3-MCPD and glycidol on Wistar Albino rat brain cells(Elsevier, 2021) Sevim, Cigdem; Ozkaraca, Mustafa; Kara, Mehtap; Ulas, Nergis; Mendil, Ali Sefa; Margina, Denisa; Tsatsakis, Aristidis3-chloropropane-1,2-diol (3-MCPD) and its toxic metabolite glycidol were classified by the International Agency for Research on Cancer (IARC) as belonging to group 2B and 2A for humans. This study aimed to determine the sub-acute toxicity of these agents. Rats were exposed to 3-MCPD at 0.87 and 10 mg/kg/bw and glycidol (2,4 and 37,5 mg/kg/bw) for 90 days. miR-21 gene expression levels significantly decreased in all group's cerebellar tissues compared with control. Exposure to 10 mg/kg/bw 3-MCPD showed significant increases in PTEN in brain as compared to control group. The Akt gen expressions were significantly decreased in 3-MCPD and glycidol groups when compared to control group brains. Additionally, Caspase 3 and AIF immunopositivity significantly increased in 3-MCPD high dose and glycidol high dose groups in cerebellum granular layers compared to control. The results of the present study conclude that 3-MCPD and glycidol can induce apoptosis in rat brain tissue.Öğe Arbutin abrogates cisplatin-induced hepatotoxicity via upregulating Nrf2/HO-1 and suppressing genotoxicity, NF-?B/iNOS/TNF-? and caspase-3/Bax/Bcl2 signaling pathways in rats(Oxford Univ Press, 2024) Okkay, Irmak Ferah; Famurewa, Ademola; Bayram, Cemil; Okkay, Ufuk; Mendil, Ali Sefa; Sezen, Selma; Ayaz, TeslimeBackground: Cisplatin is a potent anticancer agent widely employed in chemotherapy. However, cisplatin leads to toxicity on non-targeted healthy organs, including the liver. We investigated the hepatoprotective mechanism of arbutin (ARB), a glycosylated hydroquinone, against cisplatin-induced hepatotoxicity. Methods: Rats were orally administered with ARB (ARB1 = 50 mg/kg; ARB2 = 100 mg/kg) for 14 consecutive days against hepatotoxicity induced by a single dose of cisplatin (10 mg/kg) on day 15. Three days after the intraperitoneal cisplatin injection, serum and liver tissue were collected for subsequent analyses. Results: Cisplatin triggered marked increases in serum AST, ALT, and ALP activities, hepatic malondialdehyde (MDA) and reactive oxygen species (ROS) coupled with a considerable diminution in hepatic activities of superoxide dismutase (SOD), catalase (CAT) and the concentration of reduced glutathione (GSH). The gene expressions of interleukin-1 beta (IL-1 beta), tumor necrosis factor (TNF-alpha), and IL-6 were notably increased. The pre-administration of ARB1 and ARB2 reduced AST, ALT and ALP in serum and restored SOD, CAT, GSH, ROS, MDA and cytokine levels which was also evidenced by alleviated hepatic lesions. Further, cisplatin-induced prominent alterations in the gene expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), iNOS, NF-kappa B, Bax, Bcl-2, caspase-3 and 8-OHdG in the liver. Interestingly, ARB protected the liver and mitigated the cisplatin-induced alterations in serum AST, ALT, ALP, and reduced hepatic redox markers, 8-OdG, inflammatory markers and gene expressions. Conclusion: The findings demonstrate that ARB is a potential protective adjuvant against cisplatin-induced hepatotoxicity via inhibition of hepatic oxidative stress, inflammation, and apoptosis.Öğe Effects of dexpanthenol on 5-fluorouraci-induced nephrotoxicity, hepatotoxicity, and intestinal mucositis in rats: a clinical, biochemical, and pathological study(Walter De Gruyter Gmbh, 2025) Tastemur, Seyma; Ekici, Mehmet; Mendil, Ali Sefa; Ozkaraca, Mustafa; Ataseven, HilmiBackground5-fluorouracil (5-FU) is a broad-spectrum drug that has a wide range of side effects. Patients may experience severe comorbidities as a result of these toxic side effects, making it impossible for them to continue chemotherapy. Despite the fact that various molecules have been experimented, there is no literature data on the efficacy of dexpanthenol (DXP) for mitigating the toxic effects of 5-FU.ObjectiveTo investigate the protective effects of DXP on nephrotoxicity, hepatotoxicity, and intestinal toxicity induced by 5-FU in rats.MethodsTwenty-eight male Wistar-Albino rats aged 16 weeks were randomly assigned to four groups. We created a rat model of intestinal mucositis, nephrotoxicity, and hepatotoxicity through intraperitoneal 5-FU (35 mg/kg for 4 d) injection. 500 mg/kg and 1000 mg/kg of DXP were administered to the treatment groups. The effects of dexpanthenol were evaluated clinically, biochemically, histopathologically, and immunohistochemically (inducible nitric oxide synthase [iNOS], cyclooxygenase-2 [COX-2], 8-hydroxyguanosine [8-OHdG], and nuclear factor kappa B [NF-kappa B]).Results5-FU caused a decrease in body weight and food intake, and an increase in diarrhea scores in rats. 5-FU led to significant disruptions in the hepatic biochemical markers (aspartate transaminase [AST], alanine transaminase [ALT], alkaline phosphatase [ALP], total bilirubin, direct bilirubin, and lactate dehydrogenase [LDH]), renal biochemical markers (blood urea nitrogen [BUN], creatinine, and uric acid), and protein and albumin, which are markers of both hepatic and renal functions. Severe pyknosis and mononuclear cell infiltrations were observed in the liver, and mononuclear cell infiltration and tubular degeneration in the kidneys. Jejunum and colon showed villous hyperemia and hemorrhage, respectively, along with mononuclear cell infiltration. Furthermore, 5-FU increased the immunohistochemical expressions of iNOS, COX-2, 8-OHdG, and NF-kappa B in the examined tissues. The administration of DXP at doses of 500 mg/kg and 1000 mg/kg demonstrated significant mitigation of the toxic effects induced by 5-FU on the liver, kidney, jejunum, and colon.ConclusionDXP showed protective effects against nephrotoxicity, hepatotoxicity, and intestinal toxicity caused by 5-FU. These findings suggest that DXP may serve as a potential therapeutic agent to alleviate the severe side effects of 5-FU chemotherapy, thereby improving patient tolerance and quality of life. Further clinical studies are warranted to validate these results and explore the translational potential of DXP in human cancer therapy.Öğe Evaluation of 4-Hydroxy-2-Nonenal, Dityrosine and 8- Hydroxy-2-Deoxyguanosine Expressions in Lambs withWhite Muscle Disease(2021) Karakurt, Emin; Karataş, Özhan; Dag, Serpil; Beytut, Enver; Mendil, Ali Sefa; Nuhoğlu, Hilmi; Yıldız, AyferThe aim of this study was to investigate Reactive Oxygen Species (ROS)-induced lipidperoxidation, protein and DNA damage with oxidative stress markers such as 4-hydroxy-2- nonenal (4-HNE), dityrosine (DT) and 8-hydroxy-2-deoxyguanosine (8-OHdG) in lambs withWhite Muscle Disease (WMD). The material of this study consisted of tissue samples taken from20 sheep with WMD and 6 healthy control groups brought to Pathology Department for routinehistopathological diagnosis between 2012 and 2019. In macroscopic examinations, chalky-whitelarge necrotic areas on the epicardial and especially on the endocardial surfaces of the right andleft ventricular walls were observed. In microscopic examinations, it was observed that thedegenerated muscle fibers in the heart were homogeneously pink in color, lost their cytoplasmiccitration, swelled and their nuclei were pyknotic. Calcifications in necrotic and degenerated areaswere detected. All white muscle disease cases were immune positive for 4-HNE, DT and 8-OHdGexpressions in heart tissues. A significant difference (P<0.05) was detected between the groups interms of immunoreactivity to 4-HNE, DT and 8-OHdG in immunohistochemical andimmunofluorescence staining findings. In conclusion, our study showed that formation of ROS thatis important in pathogenesis of WMD causes not only lipid peroxidation, but also proteinmodification and DNA damage.Öğe Evaluation of a gold nanocomposite hyaluronic acid-based adhesion barrier withantibacterial properties in an animal model(2022) Kasımzade, Ferit; Ada, Fatih; Özkaraca, Mustafa; Mendil, Ali SefaObjectives: In this study, the effects of a gold nanocomposite hyaluronic acid-based adhesion barrier were evaluated in an animal model.\rMaterials and methods: In our study, a total of 42 rats in seven groups, with six rats in each group, were evaluated. The groups were\restablished according to the application of an adhesion barrier. In the first, second, and third groups, an adhesion barrier was applied by\rstandard median laparotomy in the first, second, and fourth weeks, respectively. The fourth, fifth, and sixth groups underwent the same\rprocedure in the first, second, and fourth weeks; however, no adhesion barrier was applied to these groups. The seventh group was the\rcontrol group, and no treatment was performed in this group.\rResults: There was no significant difference in the formation of inflammatory cells and fibrous tissue between the groups that underwent\rlaparotomy in the first and second weeks with and without the adhesion barrier (p>0.05). However, both low inflammatory cells (p<0.05)\rand low fibrous tissue (p<0.05) were evaluated in favor of the adhesion barrier group operated at the fourth week.\rConclusion: A gold nanocomposite hyaluronic acid-based adhesion barrier prevents adhesion, particularly in the long term. However, the\rresults need to be supported by clinical studies.Öğe Exploring the anti-inflammatory activity of boron compounds through the miR-21/PTEN/AKT pathway in cecal ligation and puncture-induced sepsis(Spandidos Publ Ltd, 2025) Sevim, Cigdem; Ozkaraca, Mustafa; Kara, Mehtap; Taghizadehghalehjoughi, Ali; Genc, Sidika; Yeni, Yesim; Mendil, Ali SefaThe present study investigated the impact of boric acid (BA) and borax (BX) on markers of inflammation and modifications in miR-21/PTEN/AKT pathway genes in the liver and kidney tissues of Sprague Dawley male rats with sepsis induced by cecal ligation and puncture (CLP). A total of 60 male Sprague Dawley rats were randomly divided into 6 groups, each containing 10 animals as follows: Control, CLP (where the model was created), 20 mg/kg BX (CLP + BX1), 40 mg/kg BX (CLP + BX2), 20 mg/kg BA (CLP + BA1) and 40 mg/kg BA (CLP + BA2). Liver and kidney tissues were analyzed for histopathological changes, immunopositivity for tumor necrosis factor-alpha, interleukin (IL)-6 and IL-10, and gene expression of microRNA-21 (miR-21), phosphatase and tensin homolog (PTEN) and AKT. Gene expression analysis in the liver tissues revealed a significant decrease in miR-21, and a marked but not significant decrease in PTEN levels in the CLP group, while AKT expression was significantly increased in the CLP group, and was significantly decreased in CLP + BA1 group compared with in the CLP group. In the kidney tissues, miR-21 levels were significantly decreased in the CLP group, but the CLP + BA2 group showed a significant increase compared with in the CLP group. These results suggest the potential therapeutic benefits of low-dose BA and BX in ameliorating sepsis-induced tissue damage, emphasizing the need for further exploration of their mechanisms of action.Öğe Genome-wide profiling of the expression of serum derived exosomal circRNAs in patients with hepatic alveolar echinococcosis(Elsevier, 2022) Ozdemir, Selcuk; Aksungur, Nurhak; Altundas, Necip; Kara, Salih; Korkut, Ercan; Ozkaraca, Mustafa; Mendil, Ali SefaThe patients with hepatic alveolar echinococcosis is poorly detected due to invasive and slow growth. Thus, early diagnosis of hepatic alveolar echinococcosis is so important for patients. Circular RNAs are crucial types of the non-coding RNA. Recent studies have provided serum-derived exosomal circRNAs as potential biomarkers for detection of various diseases. The clinical importance of exosomal circRNAs in hepatic alveolar echinococcosis have never been explored before. Here, we investigated the serum-derived exosomal circRNAs in the diagnosis of hepatic alveolar echinococcosis. Firstly, High-throughput Sequencing was performed using 9 hepatic alveolar echinococcosis and 9 control samples to detect hepatic alveolar echinococcosis related circRNAs. Afterwards, bioinformatic analyzes were performed to identify differentially expressed circRNAs and pathway analyzes were performed. Finally, validation of the determined circRNAs was performed using RT-PCR. The sequencing data indicated that 59 differentially expressed circRNAs; 31 up-regulated and 28 down-regulated circRNA in hepatic alveolar echinococcosis patients. The top 5 up-regulated and down-regulated circRNAs were selected for vali-dation by RT-qPCR assay. As a result of the verification, circRNAs that were significantly up-and down-regulated showed an expression profile consistent with the results obtained. Importantly, our findings suggested that identified exosomal circRNAs could be a potential biomarker for the detection of hepatic alveolar echinococcosis serum and may help to understand the pathogenesis of hepatic alveolar echinococcosis.Öğe Investigation of the miRNA levels changes to acceptable daily intake dose pesticide mixture exposure on rat mesentery and pancreas(Elsevier Ltd, 2024) Sevim, Cigdem; Tsatsakis, Aristides; Taghizadehghalehjoughi, Ali; Ozkaraca, Mustafa; Kara, Mehtap; Genc, Sidika; Mendil, Ali SefaConsumers are constantly exposed to a variety of chemical mixtures as part of their everyday activities and lifestyle. Food, water and commercial products are only some examples of the possible ways people get exposed to these mixtures. However, following federal and local guidelines for risk assessment related to chemical exposure, risk analysis focuses on a single substance exposure scenario and not on a mixture, as in real life. Realizing the pronounced gap of this methodology, the real-life risk simulation scenario approach tries to address this problem by investigating the possible effect of long-term exposure to chemical mixtures closely resembling the actual circumstances of modern life. As part of this effort, this study aimed to identify the cumulative effects of pesticides belonging to different classes and commonly used commercial products on long-term exposure with realistic doses. Sprague Dawley rats were given a pesticide mix of active ingredients and formulation chemicals in a daily acceptable dose (ADI) and 10xADI for 90 days. Following thorough everyday documentation of possible side-effects, after 90 days all animals were sacrificed and their organs were examined. Exposure to pesticides particularly affects the miRNA levels at that point will provide us with more information about whether they can be potential biomarkers. © 2023 The AuthorsÖğe Lycopene induces antiproliferative effects through apoptosis, autophagy, and oxidative DNA damage in the HeLa cells(Taylor & Francis Ltd, 2024) Parlak, Mesut; Joha, Ziad; Yulak, Fatih; Mendil, Ali Sefa; Tastemur, YasarBackground: This study explores the role of apoptosis, autophagy, and oxidative DNA damage in influencing the cytotoxic impact of lycopene on HeLa cells. Material and methods: Cell viability following exposure to varying lycopene concentrations was determined using an XTT assay. ELISA measured key cell death proteins (Bax, BCL-2, etc.), while immunofluorescence staining visualized LC3 beta (autophagy) and 8-oxo-dG (DNA damage). Results: Lycopene significantly killed HeLa cells in a dose-dependent way (IC50 = 10 mu M). Subsequent examinations conducted with the IC50 dose of lycopene demonstrated a notable elevation in the expression levels of apoptotic proteins, such as cleaved caspase 3, cleaved PARP, and Bax (p < 0.001). Additionally, treatment with this substance led to an increase in the levels of 8-oxo-dG (p < 0.001), a widely acknowledged biomarker indicative of oxidative DNA damage. Furthermore, a significant rise (p < 0.05) in LC3 beta protein levels, a well-established indicator of autophagy activation, was noted. Conclusion: This study suggests lycopene's potential to fight cervical cancer by triggering programmed cell death (apoptosis) and cellular self-digestion (autophagy). These findings highlight lycopene as a promising candidate for future cervical cancer treatments.Öğe Nobiletin reduces 5-FU-induced lung injury with antioxidative, anti-inflammatory and anti-apoptotic activities(Springer, 2025) Uslu, Gozde Atila; Uslu, Hamit; Coban, Taha Abdulkadir; Ozkaraca, Mustafa; Mendil, Ali Sefa; Aygormez, SerpilLike other chemotherapeutic agents, 5-fluorouracil (5-FU) targets cancerous cells, but it also causes many unwanted side effects on healthy tissues and cells. Based on the undesirable effects of 5-FU, the aim of this study was to determine how 5-FU affects lung tissue and whether nobiletin has any protective effect. The study consisted of negative control, Nobiletin, 5-FU and Nobiletin + 5-FU groups. Nobiletin and Nobiletin + 5-FU groups received 10 mg/kg Nobiletin i.g. for 7 days. On day 8, 100 mg/kg 5-FU was administered i.p. to 5-FU and Nobiletin + 5-FU groups. Biochemical and immunohistochemical analyses were performed on the lung tissues dissected at the end of the study. 5-FU caused growth retardation, disturbed the oxidant-antioxidant balance by increasing MDA levels and decreasing GSH levels, triggered cellular apoptosis by increasing Bax and caspase-3 levels and decreasing Bcl-2, also increased lung tissue inflammation and damage by increasing NF kappa B and IL-1 beta levels. However, it was determined that Nobiletin prevented the disruption of the oxidant-antioxidant balance, showed significant anti-apoptotic effects, especially by reducing Bax levels and partially modulating caspase-3 and Bcl-2 levels, and also exhibited anti-inflammatory effects by reducing NF kappa B and IL-1 beta levels and supported the normal development of animals. Our results showed that nobiletin pretreatment showed anti-inflammatory activity by inhibiting the NF kappa B pathway in 5-FU-induced lung injury, suppressed oxidative stress with its antioxidant activity and was effective in modulating cellular apoptosis with its anti-apoptotic activity. In conclusion, Nobiletin has been shown to have an important potential in reducing fluorouracil-induced tissue damage by acting through multiple pathways.Öğe Toxicological investigation of bisphenol A and its derivates on human breast epithelial (MCF-10A) cells(Pergamon-Elsevier Science Ltd, 2025) Bakan, Buket; Kaptaner, Burak; Tokmak, Merve; Aykut, Handan; Mendil, Ali Sefa; Ozkaraca, MustafaBisphenols can enter the body, where they have potential adverse effects on human health, via different routes such as inhalation, dermally or orally. They are known as endocrine disrupting chemicals that activate signaling pathways by mimicking the estrogen actions. In this study, we aimed to investigate effects of bisphenol A (BPA), and its analogues bisphenol F (BPF) and bisphenol S (BPS) on MCF-10A cells and their impact mechanisms on autophagy, apoptosis and reduced glutathion levels. In comparison of the cytotoxic effects, while BPF and BPS showed dose-dependent high toxicity on MCF-10A cells, BPA exerted cytotoxic effects only at the highest doses. Caspase 3 and LC3B are strongly and positively correlated with BPF exposures while significant changes were not detected in the BPA and BPS applied groups. It was clearly observed that BPF and BPS displayed more toxic effects than BPA on human breast cells that are important targets for the bisphenols. These findings provide data for understanding the mechanisms for BPA, BPF and BPS-induced toxicity on human breast cells.
