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Updated: May 12, 2026
06:58
Synthesis of an In vivo MRI-detectable Apoptosis Probe
Published on: July 31, 2012
Contrast agents and renal cell apoptosis.
Giulia Romano1, Carlo Briguori, Cristina Quintavalle
1Department of Cellular and Molecular Biology and Pathology, Federico II University of Naples, Naples, Italy.
European Heart Journal
|May 13, 2008
Summary
Contrast media (CM) cause dose-dependent kidney cell apoptosis. N-acetylcysteine (NAC) and ascorbic acid, but not sodium bicarbonate, protect against this contrast-induced kidney damage.
Area of Science:
- Nephrology
- Toxicology
- Cell Biology
Background:
- Contrast media (CM) can cause direct toxic effects on renal tubular cells.
- This toxicity is implicated in the pathophysiology of contrast nephropathy.
Purpose of the Study:
- To evaluate the cytotoxicity of low-osmolality (LOCM) and iso-osmolality (IOCM) contrast media on renal cells.
- To assess the protective effects of antioxidants against contrast-induced nephrotoxicity.
Main Methods:
- Assessed cytotoxicity of CM, iodine, and mannitol on human embryonic kidney (HEK 293), porcine LLC-PK1, and canine MDCK cells.
- Evaluated cell viability, DNA laddering, flow cytometry, and caspase activation.
- Tested n-acetylcysteine (NAC), ascorbic acid, and sodium bicarbonate for protective effects.
Main Results:
- Both LOCM and IOCM induced dose- and time-dependent cell death, activating apoptosis via the intrinsic pathway.
- No significant difference in cytotoxicity was observed between LOCM and IOCM.
- NAC and ascorbic acid demonstrated a dose-dependent protective effect against CM-induced renal cell apoptosis.
Conclusions:
- Both LOCM and IOCM trigger dose-dependent apoptosis in renal cells.
- NAC and ascorbic acid effectively prevent contrast-induced apoptosis, while sodium bicarbonate does not.
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