Browsing by Author "Ozkaraca, Mustafa"

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Effectiveness of Hesperidin on Methotrexate-Induced Testicular Toxicity in Rats
(Kafkas Univ, veteriner Fakultesi dergisi, 2017) Belhan, Saadet; Ozkaraca, Mustafa; Kandemir, Fatih Mehmet; Gulyuz, Fetih; Yildirim, Serkan; Omur, Ali Dogan; Yener, Zabit
The aim of this study was to investigate the effect of hesperidin on male reproductive system in rats to which methotrexate (MTX) was administered. In the study, 28 male Wistar albino rats at the age of 8 weeks and had 250-300 g of live weight were used. Four experimental groups were formed; Group 1 (n=7): The control group, only feed and water were given. Group 2 (n=7): MTX group, a single dose of 20 mg/kg of i.p. MTX was administered. Group 3 (n=7): Hesperidin group, 200 mg/kg of hesperidin was administered by gavage for 7 days. Group 4: MTX + hesperidin group (n=7): Following administration of a single dose of 20 mg/kg i.p. MTX, 200 mg/kg of Hesperidin was administered by oral gavage for 7 days. At the end of the experiment, rats were decapitated and biochemical, histopathological and spermatological parameters were examined. It was observed that in the MTX group, sperm motility and density, the enzymes CAT, GPx and SOD and GSH level decreased, TNF-alpha and IL-1 Beta, as well as MDA, levels were increased, regular structure of spermatogenic cells was impaired, and seminiferous tubules became necrotic and degenerative. It was determined that spermatological parameters improved and, necrotic and degenerative changes diminished by the administration of MTX+hesperidin. These outcomes indicated that hesperidin had a protective effect on destructive effects of MTX in rat testiclesv.
Neurotoxic Responses in Brain Tissues of Rainbow Trout Exposed To Imidacloprid Pesticide: Assessment of 8-Hydroxy Activity, Oxidative Stress and Acetylcholinesterase Activity
(Pergamon-elsevier Science Ltd, 2017) Topal, Ahmet; Alak, Gonca; Ozkaraca, Mustafa; Yeltekin, Ash Cilingir; Comakli, Selim; Acil, Gurdal; Atamanalp, Muhammed
The extensive use of imidacloprid, a neonicotinoid insecticide, causes undesirable toxicity in non targeted organisms including fish in aquatic environments. We investigated neurotoxic responses by observing 8-hydroxy-2-deoxyguanosine (8-OHdG) activity, oxidative stress and acetylcholinesterase (AChE) activity in rainbow trout brain tissue after 21 days of imidacloprid exposure at levels of (5 mg/L, 10 mg/L, 20 mg/L). The obtained results indicated that 8-OHdG activity did not change in fish exposed to 5 mg/L of imidacloprid, but 10 mg/L and 20 mg/L of imidacloprid significantly increased 8-OHdG activity compared to the control (p < 0.05). An immunopositiv reaction to 8-OHdG was detected in brain tissues. The brain tissues indicated a significant increase in antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)) compared to the control and there was a significant increase in malondialdehyde (MDA) levels (p < 0.05). High concentrations of imidacloprid caused a significant decrease in AChE enzyme activity (p < 0.05). These results suggested that imidacloprid can be neurotoxic to fish by promoting AChE inhibition, an increase in 8-OHdG activity and changes in oxidative stress parameters. Therefore, these data may reflect one of the molecular pathways that play a role in imidacloprid toxicity. (C) 2017 Elsevier Ltd. All rights reserved.
Protective Role of Chrysin on Doxorubicin-Induced Oxidative Stress and Dna Damage in Rat Testes
(Wiley, 2020) Belhan, Saadet; Ozkaraca, Mustafa; Ozdek, Ugur; Komuroglu, Ahmet Ufuk
This study investigated the role of chrysin (CR) in DNA damage likely to occur in the testicle and oxidative stress caused by doxorubicin (DXR). Twenty-eight rats were divided into four groups as control, DXR, DXR + CR and CR groups. Sperm parameters, oxidative status, testicular biopsy score, DNA damage and plasma testosterone levels were analysed. Noticeable reductions in sperm count, motility and testosterone were detected in the DXR group compared to controls. In addition, significant increases in malondialdehyde (MDA), catalase (CAT) and glutathione (GSH) levels, and in abnormal sperm rates were detected. Severe degenerative changes occurred in the tubules of DXR rat testes; the inter-tubular areas were oedematous. Immunofluorescence staining was conducted with 8-OhDG (8 oxo-2 '-deoxyguanosine) to evaluate DNA damage, and severe positivity was found in tubular gaps in the DXR rat testes. When the DXR + CR group was compared with the DXR group, the abnormal sperm rate was found to have decreased significantly. Positivity in the tubular space and degenerative changes in the seminiferous tubules were also diminished. We recommend the administration of CR with DXR to reduce the possible adverse effects of DXR, a medicine preferred in cancer therapy.
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, Mustafa
Bisphenols 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.