The Effects of Vitamin D Application on NaF-Induced Cytotoxicity in Osteoblast Cells (hFOB 1.19).

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Dede S., Taşpinar M., Yüksek V., Çetin S., Usta A.

Biological trace element research, cilt.201, sa.2, ss.698-705, 2023 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 201 Sayı: 2
  • Basım Tarihi: 2023
  • Doi Numarası: 10.1007/s12011-022-03177-8
  • Dergi Adı: Biological trace element research
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Aqualine, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Food Science & Technology Abstracts, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Sayfa Sayıları: ss.698-705
  • Anahtar Kelimeler: Osteoblast, NaF, Vitamin D, Cytotoxicity
  • Van Yüzüncü Yıl Üniversitesi Adresli: Evet

Özet

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-∆∆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, 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 (6-fold) 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.