Non-Ionic Contrast Media Induces Oxidative Stress and Apoptosis Through Ca2+ Influx in Human Neutrophils


KAYAN M., NAZIROĞLU M., Ovey I. S. , Aykur M. , Uguz A. C. , YÜREKLİ V. A.

JOURNAL OF MEMBRANE BIOLOGY, cilt.245, ss.833-840, 2012 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 245 Konu: 12
  • Basım Tarihi: 2012
  • Doi Numarası: 10.1007/s00232-012-9491-x
  • Dergi Adı: JOURNAL OF MEMBRANE BIOLOGY
  • Sayfa Sayıları: ss.833-840

Özet

Non-ionic contrast media (CM) can induce tissue kidney injury via activation of phagocytosis and oxidative stress, although the mechanisms of injury via neutrophils are not clear. We investigated the effects of CM on oxidative stress and Ca2+ concentrations in serum and neutrophils of humans. Ten migraine patients were used in the study. Serum and neutrophil samples from patients' peripheral blood were obtained before (control) and 30 min after non-ionic (iopromide) CM injection. The neutrophils were incubated with non specific transient receptor potential 2 (TRPM2) channel blocker, 2-aminoethoxydiphenyl borate (2-APB), and voltage gated Ca2+ channel blockers, verapamil plus diltiazem. Serum and neutrophil lipid peroxidation, apoptosis and intracellular Ca2+ concentrations levels were higher in the CM group than in controls. The neutrophilic reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) levels as well as serum vitamin E and beta-carotene concentrations were lower in the CM group than in controls. Neutrophil lipid peroxidation levels were lower in the CM+2-APB and CM+verapamil-diltiazem groups than in the CM group, although GSH, GSH-Px and intracellular Ca2+ values increased in the CM+2-APB and CM+verapamil-diltiazem groups. However, caspase-3, caspase-9, vitamin A and vitamin C values were unaltered by CM treatment. In conclusion, we observed that CM induced oxidative stress and Ca2+ influx by decreasing vitamin E, beta-carotene and Ca2+ release levels in human serum and neutrophils. However, we observed protective effects of Ca2+ channel blockers on Ca2+ influx in neutrophils.