Effects of Selenium on Calcium Signaling and Apoptosis in Rat Dorsal Root Ganglion Neurons Induced by Oxidative Stress


Uguz A. C. , NAZIROĞLU M.

NEUROCHEMICAL RESEARCH, cilt.37, ss.1631-1638, 2012 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 37 Konu: 8
  • Basım Tarihi: 2012
  • Doi Numarası: 10.1007/s11064-012-0758-5
  • Dergi Adı: NEUROCHEMICAL RESEARCH
  • Sayfa Sayısı: ss.1631-1638

Özet

Ca2+ is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca2+ overload is detrimental to cellular function and may present as an important cause of cellular oxidative stress generation and apoptosis. The aim of this study is to investigate the effects of selenium on lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (GSH-Px), cytosolic Ca2+ release, cell viability (MTT) and apoptosis values in dorsal root ganglion (DRG) sensory neurons of rats. DRG cells were divided into four groups namely control, H2O2 (as a model substance used as a paradigm for oxidative stress), selenium, selenium + H2O2. Moderate doses and times of H2O2 and selenium were determined by MTT test. Cells were preterated 200 nM selenium for 30 h before incubatation with 1 mu M H2O2 for 2 h. Lipid peroxidation levels were lower in the control, selenium, selenium + H2O2 groups than in the H2O2 group. GSH-Px activities were higher in the selenium groups than in the H2O2 group. GSH levels were higher in the control, selenium, selenium + H2O2 groups than in the H2O2 group. Cytosolic Ca2+ release was higher in the H2O2 group than in the control, selenium, selenium + H2O2 groups. Cytosolic Ca2+ release was lower in the selenium + H2O2 group than in the H2O2. In conclusion, the present study demonstrates that selenium induced protective effects on oxidative stress, [Ca2+](c) release and apoptosis in DRG cells. Since selenium deficiency is a common feature of oxidative stress-induced neurological diseases of sensory neurons, our findings are relevant to the etiology of pathology in oxidative stress-induced neurological diseases of the DRG neurons.