The Journal of Membrane Biology

, Volume 246, Issue 2, pp 91–100

Role of Contrast Media on Oxidative Stress, Ca2+ Signaling and Apoptosis in Kidney

Authors

    • Department of Biophysics, Faculty of MedicineSüleyman Demirel University
  • Neslihan Yoldaş
    • Faculty of MedicineSüleyman Demirel University
  • Esra Nur Uzgur
    • Faculty of MedicineSüleyman Demirel University
  • Mustafa Kayan
    • Department of Radiology, Faculty of MedicineSüleyman Demirel University
Article

DOI: 10.1007/s00232-012-9512-9

Cite this article as:
Nazıroğlu, M., Yoldaş, N., Uzgur, E.N. et al. J Membrane Biol (2013) 246: 91. doi:10.1007/s00232-012-9512-9

Abstract

Contrast media (CM)-induced nephropathy is a common cause of iatrogenic acute renal failure. The aim of the present review was to discuss the mechanisms and risk factors of CM, to summarize the controlled studies evaluating measures for prevention and to conclude with evidence-based strategies for prevention. A review of the relevant literature and results from recent clinical studies as well as critical analyses of published systematic reviews used MEDLINE and the Science Citation Index. The cytotoxicity induced by CM leads to apoptosis and death of endothelial and tubular cells and may be initiated by cell membrane damage together with reactive oxygen species (ROS) and inflammation. Cell damage may be aggravated by factors such as tissue hypoxia, properties of individual CM such as ionic strength, high osmolarity and/or viscosity. Clinical studies indeed support this possibility, suggesting a protective effect of ROS scavenging with the administration of N-acetylcysteine, ascorbic acid erdosteine, glutathione and bicarbonate infusion. The interaction between extracellular Ca2+, which plays a central role in intercellular contacts and production of ROS, and the in vitro toxicity of CM was also reviewed. The current review addresses the role of oxidative stress in the pathogenesis of CM in the kidney as well as current and potential novel treatment modalities for the prevention of neutrophil activation and CM-induced kidney degeneration in patients. ROS production through CM-induced renal hypoxia may exert direct tubular and vascular endothelial injury. Preventive strategies via antioxidant supplementation include inhibition of ROS generation or scavenging.

Keywords

ApoptosisRadiocontrast mediaCalcium ionOxidative stressMitochondria

Abbreviations

CAT

Catalase

CM

Contrast media

GSH-Px

Glutathione peroxidase

MDA

Malonyl dialdehyde

NAC

N-acetyl cysteine

ROS

Reactive oxygen substances

SOD

Superoxide dismutase

XO

Xanthine oxidase

Copyright information

© Springer Science+Business Media New York 2012