Doxorubicin toxicity in the Iron Age

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Item Type:	Editorial
Title:	Doxorubicin toxicity in the Iron Age
Creators Name:	Luft, F.C.
Abstract:	Anthracyclines, such as doxorubicin, are cardiotoxic. Their administration may result in a refractory form of heart failure; the mechanism is imperfectly defined, although altered intracellular iron metabolism appears to play a role. In this issue, Corna et al. investigated the notion that iron regulatory protein 1 (IRP1) might mediate doxorubicin toxicity [1]. They gave doxorubicin to wild-type and IRP1 gene-deficient mice. The mice down-regulated iron regulatory protein 2 (IRP2) but got sick anyway. The authors conclude that doxorubicin toxicity occurs independently of IRB1. Their precise electrophoretic mobility shift assays, Western blots, Northern blot analyses, oxidative stress estimates, and brain natriuretic peptide read-outs convince the hardened basic scientist, not to mention the naive clinician. In terms of doxorubicin toxicity, we remain the oxen standing in front of the mountain; we have not gotten very much smarter. However, perhaps we clinicians, who after all must prescribe the anthracyclines, should have another look at doxorubicin toxicity, the IRP molecules, and their function. [beginning of text]
Source:	Journal of Molecular Medicine
ISSN:	0946-2716
Publisher:	Springer
Volume:	84
Page Range:	529-531
Date:	July 2006
Official Publication:	https://doi.org/10.1007/s00109-006-0069-x
PubMed:	View item in PubMed

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