The sulfite molecule enhances homocysteine toxicity in SH-SY5Y cells

GÜNDOĞDU G., DODURGA Y., KÜÇÜKATAY V.

MOLECULAR BIOLOGY REPORTS, cilt.46, sa.4, ss.4017-4025, 2019 (SCI-Expanded, Scopus) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 46 Sayı: 4
  • Basım Tarihi: 2019
  • Doi Numarası: 10.1007/s11033-019-04850-3
  • Dergi Adı: MOLECULAR BIOLOGY REPORTS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.4017-4025
  • Anahtar Kelimeler: Homocysteine, Sulfite, Neurotoxicity, Neurodegenerative diseases, OXIDATIVE STRESS, NEURODEGENERATIVE DISEASES, PLASMA HOMOCYSTEINE, ALZHEIMERS-DISEASE, HYPERHOMOCYSTEINEMIA, METABOLISM, BETA, NEUROTOXICITY, HIPPOCAMPUS, DEFICIENCY
  • Atatürk Üniversitesi Adresli: Evet

Özet

Homocysteine (hcy) is an amino acid that contains sulfur species. In healthy individuals, plasma hcy levels are low. The aim of this study was to investigate the potential neurotoxic effects of hcy and sulfite (sft) molecules alone and in their combination, and also to identify the relationship of these substances on oxidative stress. SH-SY5Y cells were used as an invitro neurodegenerative disease model. The SH-SY5Y cells were treated with various concentrations of hcy alone, sft alone (final concentrations in the well were 10-250 mu M and 0.1-5mM, respectively) and a combination of both (hcy+sft). Their cytotoxicity and genotoxic effects were investigated using the XTT test and Comet assay and, their impact on oxidative stress was examined using total antioxidant-oxidant status(TAS-TOS) kits. The highest toxic doses of hcy and sft were found to be 250 mu M and 5mM, respectively, but the maximum toxic effect was observed for hcy+sft (p<0.001). In addition, an increase in DNA damage was evident in all groups, but maximal damage was inflicted using in hcy+sft (p<0.001). The oxidative stress index was significantly increased in hcy+sft (p<0.05). Determining the increase in sft and hcy levels may contribute to delaying the occurrence of diseases before symptoms of neurodegenerative disease appear.