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    Phototherapy causes a transient DNA damage in jaundiced newborns
    (INFORMA HEALTHCARE, 2013) Kahveci, Hasan; Dogan, Hasan; Karaman, Ali; Caner, Ibrahim; Tastekin, Ayhan; Ikbal, Mevlit
    In this study, we aimed to clarify the following questions: 1) Does phototherapy (PT) cause genotoxicity in full-term newborn babies undergoing PT as a result of neonatal jaundice?, 2) if genotoxic effect occurs, is there any relationship between the duration of PT and genotoxicity?, and 3) is genotoxic effect temporary or not? The frequency of sister chromatid exchange (SCE) was determined in jaundiced newborns before, during, and after phototherapy, then determined again in childhood (approximately 3.5 years old). Mean frequency of SCE of 22 full-term jaundiced babies significantly increased during the PT procedure and in every single day, compared to the previous day, in comparison to the pre-PT basal value (6.20 +/- 0.57;); mean SCE frequencies at 24, 48, 72, and 96 hours were 7.75 +/- 0.40, 8.16 +/- 0.47, 8.50 +/- 0.40, and 9.36 +/- 0.55, respectively (all P-values < 0.01). In childhood, no significant difference was found between the mean SCE value (4.9 +/- 0.9) of 20 of 22 children, who received PT in the neonatal period, and the mean SCE value (4.7 +/- 0.6) of 20 coevaluated healthy children (P = 0.40). This study demonstrates that the negative effect of PT on SCE is a temporary effect.
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    Pyridoxine may protect the cerebellar granular cells against glutamate-induced toxicity
    (VERLAG HANS HUBER, 2007) Bueyuekokuroglu, Mehmet Emin; Gepdiremen, Akcahan; Tastekin, Ayhan; Ors, Rahmi
    In the present study, the possible protective effect of the pyridoxine against glutamate-induced neurotoxicity in cerebellar granular cell culture of rat pups is investigated for its therapeutic potential. Glutamate (10(-7) M) was administered to cerebellar granular cell cultures that were prepared from one-day-old Sprague-Dawley rats. The neuroprotective effect of pyridoxine was examined. Pyridoxine at the doses of 10(-8), 10(-7), 10(-6), and 10(-5) M was introduced into the culture flasks before inclusion of glutamate. Pyridoxine at the doses of 10(-8) M and 10(-7) M significantly reduced glutamate cytotoxicity. A 10(-7) M dose of pyridoxine proved to be more effective than a 10(-8) M dose. The present study demonstrates that pyridoxine may protect glutamate-induced neurotoxicity. Neuroprotective effect of pyridoxine, at least in part, may result from its anti-glutamatergic activity. Pyridoxine merits further investigation as a therapeutic option in hypoxic-ischemic brain injury.