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    In vitro evaluation of the apoptotic, autophagic, and necrotic molecular pathways of fluoride
    (Humana Press, 2021) Urut, F.; Dede, Semiha; Yüksek, Veysel; Çetin, Sedat; Usta, Ayşe; Taşpınar, Mehmet
    The original version of this article unfortunately contained mistakes. The complete list of corrections is given below. & The author’s affiliations in now corrected in the author group. & The correct order of the keywords should be: Apoptosis, Autophagy, In vitro, Naf, Necrosis, NRK-52E cell line & p.2, fourth sentence of the last paragraph under the header “Total RNA Isolation and Quantitative Real-Time PCR”, BCt should be CT & p.3, second sentence of the first paragraph under the Results section, results should be PCR results & The correct bibliographic information for reference [1] should be Yur F, Mert N, Dede S, Değer Y, Ertekin A, Mert H, Yaşar S, Doğan I, Işık A (2013) Evaluation of serum lipid fractions and tissue antioxidant levels in sheep with fluorosis. Fluoride 46(2):90–96
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    The effects of vitamin D application on NaF-Induced Cytotoxicity in Osteoblast Cells (hFOB 1.19)
    (Humana Press, 2023) Dede, Semiha; Taşpınar, Mehmet; Yüksek, Veysel; Çetin, Sedat; Usta, Ayşe
    This study was planned to evaluate the effect of vitamin D administration on cytotoxicity due to fluoride exposure in vitro. NaF (IC50) and vitamin D (proliferative) were applied to human osteoblast (hFOB 1.19) cells. The major genes of apoptotic, autophagic, and necrotic pathways were determined by RT-PCR. 2-Delta Delta Ct formulation was used for expression analysis. In the NaF group, caspase 3, Bax, Bad, Bak, Bclx, Atg3, Atg5, Atg6, pG2, LC3-I, LC3-II, RIP1, and RIP3 genes were increased (2.6-15 times). It was observed that the expressions of these genes approached the control when vitamin D was given together with NaF. The Bcl2 gene increased significantly (sixfold) with the effect of NaF, and was down-regulated to some extent with additional vitamin D administration, but still more than in the control. As a result, it was determined that apoptotic, necrotic, and autophagic pathways were activated as the molecular basis of the damage in the bone tissue, which was most affected by fluorine, and these genes were down-regulated and approached the control group with the addition of vitamin D. It was concluded that this is an important data to explain the molecular basis of the protective and therapeutic effect of vitamin D against fluorine toxicity.
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    Vitamin D may assist the UPR against sodium fluoride-induced damage by reducing RIPK1, ATG5, BECN1, oxidative stress and increasing caspase-3 in the osteoblast MC3T3-E1 cell line
    (Elsevier GmbH, 2023) Yüksek, Veysel; Dede, Semiha; Çetin, Sedat; Usta, Ayşe; Taşpınar, Mehmet
    Out of all measure systemic exposure to fluorides can cause defect of skeletal and dental fluorosis. Endoplasmic reticulum (ER) stress is caused by fluorine-induced oxidative stress and importance of vitamin D in its prevention is not known enough in bone cells. This study was carried out to investigate fluorine-induced oxidative stress, ER stress, and death pathways and the effect of vitamin D on them. Methods: MC3T3-E1 mouse osteoblast cell line was used as the material of the study. The NaF and vitamin D concentrations were determined by the MTT assay. NaF treatments and vitamin D supplementation (pre-add, co-add, and post-add) was administered in the cell line at 24th and 48th hours. The expression of the genes in oxidative stress, ER stress, and death pathways was determined using RT-qPCR and Western blotting techniques. Results: Vitamin D significantly reduced mRNA expression levels of SOD2, CYGB, ATF6, PERK, IRE1, ATG5 and BECN1 whereas caused an increase in levels GPX1, SOD1, NOS2 and Caspase-3 in MC3T3-E1 mouse osteoblast cell line of NaF-induced. In addition, GPX1, SOD1, ATF6, PERK, IRE1, BECN1, Caspase-3 and RIPK1 protein levels were examined by Western blot analysis, and it was determined that vitamin D decreased IRE1 and PERK protein levels, but increased GPX1, SOD1, ATF6 and Caspase-3 protein levels. Conclusion: The findings of the study suggest that vitamin D has protective potential against NaF-induced cytotoxicity reasonably through the attenuation of oxidative stress, ER stress, ATG5, IRE1 and by increasesing caspase-3 in vitro conditions.