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    Melatonin attenuates caspase-dependent apoptosis in the thoracic aorta by regulating element balance and oxidative stress in pinealectomised rats
    (Canadian Science Publishing, 2019) Doganlar, Zeynep Banu; Uzun, Metehan; Ovali, Mehmet Akif; Dogan, Ayten; Ongoren, Gulin; Doganlar, Oguzhan
    The aim of this study was to explain the possible mechanisms by which melatonin deficiency results in cardiovascular injury and to investigate the effects of melatonin administration on important signalling pathways and element equilibrium in the thoracic aorta (TA). For this purpose, we analysed the cellular and molecular effects of melatonin deficiency or administration on oxidative stress, DNA damage, molecular chaperone response, and apoptosis induction in TA tissues of pinealectomised rats using ELISA, RAPD, qRT-PCR, and Western blot assays. The results showed that melatonin deficiency led to an imbalance in essential element levels, unfolded or misfolded proteins, increased lipid peroxidation, and selectively induced caspasedependent apoptosis in TA tissues without significantly affecting the Bcl-2/BAX ratio (2.28 in pinealectomised rats, 2.73 in pinealectomised rats treated with melatonin). In pinealectomised rats, the genomic template stability (80.22%) was disrupted by the significantly increased oxidative stress, and heat shock protein 70 (20.96-fold), TNF-alpha (1.73-fold), caspase-8 (2.03-fold), and caspase-3 (2.87-fold) were markedly overexpressed compared with the sham group. Melatonin treatment was protective against apoptosis and inhibited oxidative damage. In addition, melatonin increased the survivin level and improved the regulation of element equilibrium in TA tissues. The results of the study indicate that melatonin deficiency induces TNF-alpha-related extrinsic apoptosis signals and that the administration of pharmacological doses of melatonin attenuates cardiovascular toxicity by regulating the increase in the rate of apoptosis caused by melatonin deficiency in TA tissue of Sprague-Dawley rats.
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    Potential Biomarkers for Melatonin Deficiency in Thoracic Aorta and Left Ventricle of Pinealectomised Rats
    (Wiley-Blackwell, 2015) Doganlar, Oguzhan; Uzun, Metehan; Doganlar, Zeynep Banu; Ovali, Mehmet Akif; Ongoren, Gulin
    [Abstract Not Available]
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    SINGLE AND COMBINED TOXICITY OF ALUMINIUM AN AZORUBINE: PHYSIOLOGICAL AND GENETIC RESPONSES OF DROSOPHILA MELANOGASTER
    (Parlar Scientific Publications (P S P), 2017) Doganlar, Oguzhan; Doganlar, Zeynep Banu; Ongoren, Gulin; Kahraman, Ozge; Altinoluk, Pinar; Kirbas, Asude
    This study aimed that investigation of the toxic effects of Aluminum (Al) and Azorubine. Adult D. melanogaster flies were treated with Al (100, 200 and 400 ppb) and Azorubine (50 ppm) at both single and combined for 1 and 5 days. The concentrations were selected based on permitted limits in drinking water for Al (200 ppb) and food for Azorubine (50 ppm), respectively. The accumulations of Al and Azorubine, mRNA levels of antioxidant enzymes (superoxide dismutase, catalase and glutathione synthase), heat shock proteins (HSP26, 60, 70 and 83) as well as octopamine levels were determined. RAPD analysis was also performed in order to determine genomic template stability (GTS%). Azorubine addition caused increasing take up the Al, decreasing expressions of antioxidant enzymes and changes in the HSP expression patterns. GTS was decreased with the increased treatment time. The minimum GTS was determined at the 400 ppb Al and Azorubine alone treatment at the both exposure time. The higher increase of the octopamine (4.83 fold) was determined at the 100 ppb Al+Azorubine and 400 ppb Al+Azorubine (3.73 -fold) at the fifth day. We conclude that permitted limits of Al and Azorubine (both single and combined) may cause toxic effects on molecular and physiological level.