Yazar "Ozerol, Beyza Guzide" seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim Yok
    Öğe
    Effect of perinatal nicotine exposure on oxidative stress and BDNF levels in the brain tissue of offspring rats: The protective role of Vitamin E
    (Churchill Livingstone, 2025) Ozerol, Beyza Guzide; Selcuk, Engin Burak; Gurel, Elif; Uremis, Muhammed Mehdi; Gul, Mehmet; Gul, Semir; Bag, Harika Gozde Gozukara
    Objective: Nicotine, a well-known neurotoxin, induces oxidative stress in fetal tissues, leading to organ damage and fetal growth retardation. This study aims to evaluate oxidative stress parameters in the brain tissue of rat offspring exposed to perinatal nicotine and assess vitamin E's protective effects. Methods: Twenty-five pregnant rats were administered 10 mg/L of nicotine and 300 mg/L of Vitamin E in drinking water starting from the first day of gestation. On gestational day 21, some offspring were euthanized to form the prenatal group. The remaining litters were born naturally, and dams received treatments via drinking water during gestation and lactation (6 weeks). After the lactation period, the pups were weaned and directly treated for an additional 9 weeks, resulting in an overall treatment duration of 15 weeks. Brain tissues were analyzed for MDA, GSH, TOS, TAS, OSI, BDNF, Caspase-3 activity, and histopathological changes. Results: The nicotine-exposed pups exhibited significantly reduced crown-rump length, body mass, and brain mass compared to controls. Nicotine exposure decreased BDNF, GSH, and TAS levels and increased MDA, TOS, and OSI levels. Histopathologically, the nicotine prenatal group showed a significantly higher number of heterochromatic nuclei in brain tissue. Caspase-3 activity did not show a significant increase in nicotine groups compared to the control. Vitamin E supplementation mitigated nicotine-induced brain damage in some measured parameters. Conclusion: Perinatal nicotine exposure induces oxidative damage in the brain tissue of rat offspring, while vitamin E exerts a protective antioxidant effect, preventing nicotine-induced neurotoxicity. Furthermore, the significant reduction in BDNF levels and the increase in heterochromatic nuclei in the nicotine-exposed groups highlight the detrimental impact of nicotine on neurodevelopment, which can be effectively mitigated by vitamin E supplementation.
  • Küçük Resim Yok
    Öğe
    Protective effect of dexpanthenol against methotrexate-induced liver oxidative toxicity in rats
    (Taylor & Francis Ltd, 2023) Gurler, Mukaddes; Selcuk, Engin Burak; Ozerol, Beyza Guzide; Tanbek, Kevser; Taslidere, Elif; Yildiz, Azibe; Yagin, Fatma Hilal
    Methotrexate is a familiar chemotherapeutic preferred in a wide range of clinical fields such as leukemia, psoriasis, rheumatoid arthritis, neoplastic and autoimmune disorders. However, methotrexate therapy has limitations as it causes severe side effects from which liver damage is the most important one. Several antioxidant compounds have been studied against methotrexate related liver toxicity, but dexpanthenol has not been experienced. Vitamin B5-derived dexpanthenol is a usual therapeutic having a potent anti-inflammatory and antioxidant effect. In this study, we aimed to evaluate the ameliorating effect of dexpanthenol against methotrexate-induced hepatotoxicity. We performed our experiments on Wistar albino rats divided randomly into four groups involving control, dexphantenol, dexpanthenol + methotrexate and methotrexate applied animals. After this experimental work on rats, for the first time, we showed dexpanthenol improvement effect on ROS-caused hepatotoxicity initiated by methotrexate administration in terms of liver tissue antioxidant/oxidant enzymes, liver function tests, and histological changes. We suggest that dexpanthenol might be applied during methotrexate treatment in order to reduce the liver toxicity. However, further studies are needed to find out the optimal dose regimen and to understand the mechanism of action.