Gadodiamide Induced Autophagy and Apoptosis in Human Keratinocytes

Background/Aim: Gadolinium has been reported to cause liver lobular necrosis and nephrogenic systemic fibrosis. However, its toxicity to the skin remains unknown. This study aimed to investigate the effect of a high dose of gadolinium-based contrast agent gadodiamide on the human keratinocyte HaCaT cell line. Materials and Methods: Cell viability was assessed using MTT assay, and autophagy was assessed using acridine orange and LysoTracker Red staining. Western blotting was performed to verify the changes in Bcl2 and Bax levels. Results: The viability of HaCaT cells was significantly suppressed after gadodiamide treatment. Interestingly, gadodiamide caused autophagic vacuoles, whereas the autophagy inhibitors 3-methyladenine and chloroquine significantly alleviated autophagic cell which was reduced by caspase inhibitors. Gadodiamide also inhibited Bcl-2 expression and promoted Bax expression. Conclusion: Gadodiamide induced both autophagy and apoptosis in HaCaT cells. Physicians should carefully assess the gadodiamide dosage used clinically.

Automated summary

This study investigates the effect of gadodiamide, a gadolinium-based contrast agent, on human keratinocytes. The results show that gadodiamide treatment significantly reduces cell viability and induces both autophagy and apoptosis in HaCaT cells. The expression of Bcl-2 is inhibited while the expression of Bax is promoted by gadodiamide.