β-carotene treatment alters the cellular death process in oxidative stress-induced K562 cells


Akçakaya H., Tok S., Dal F., ÇINAR S., Nurten R.

Cell Biology International, cilt.41, sa.3, ss.309-319, 2017 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 41 Sayı: 3
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1002/cbin.10727
  • Dergi Adı: Cell Biology International
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.309-319
  • Anahtar Kelimeler: apoptosis, cancer, cell death, mitochondria, oxidative stress
  • İstanbul Yeni Yüzyıl Üniversitesi Adresli: Hayır

Özet

Oxidizing agents (e.g., H2O2) cause structural and functional disruptions of molecules by affecting lipids, proteins, and nucleic acids. As a result, cellular mechanisms related to disrupted macro molecules are affected and cell death is induced. Oxidative damage can be prevented at a certain point by antioxidants or the damage can be reversed. In this work, we studied the cellular response against oxidative stress induced by H2O2 and antioxidant–oxidant (β-carotene–H2O2) interactions in terms of time, concentration, and treatment method (pre-, co-, and post) in K562 cells. We showed that co- or post-treatment with β-carotene did not protect cells from the damage of oxidative stress furthermore co- and post-β-carotene-treated oxidative stress induced cells showed similar results with only H2O2 treated cells. However, β-carotene pre-treatment prevented oxidative damage induced by H2O2 at concentrations lower than 1,000 μM compared with only H2O2-treated and co- and post-β-carotene-treated oxidative stress-induced cells in terms of studied cellular parameters (mitochondrial membrane potential [Δψm], cell cycle and apoptosis). Prevention effect of β-carotene pre-treatment was lost at concentrations higher than 1,000 μM H2O2 (2–10 mM). These findings suggest that β-carotene pre-treatment alters the effects of oxidative damage induced by H2O2 and cell death processes in K562 cells.