Abstract
The cumulative cardiac toxicity of the anthracycline antibiotics and their propensity to produce severe tissue injury following extravasation from a peripheral vein during intravenous administration remain significant problems in clinical oncologic practice. Understanding of the free radical metabolism of these drugs and their interactions with iron proteins led to the development of dexrazoxane, an analogue of EDTA with intrinsic antineoplastic activity as well as strong iron binding properties, as both a prospective cardioprotective therapy for patients receiving anthracyclines and as an effective treatment for anthracycline extravasations. In this review, the molecular mechanisms by which the anthracyclines generate reactive oxygen species and interact with intracellular iron are examined to understand the cardioprotective mechanism of action of dexrazoxane and its ability to protect the subcutaneous tissues from anthracycline-induced tissue necrosis.
Keywords: Dexrazoxane, anthracycline, doxorubicin, oxidative stress, iron, chelator, cardiac toxicity, extravasation injury, cumulative cardiac toxicity, antineoplastic activity, oxygen species, tissue necrosis, daunorubicin, non-Hodgkin’s lymphoma, tissue injury.
Current Pharmaceutical Biotechnology
Title:Dexrazoxane for the Prevention of Cardiac Toxicity and Treatment of Extravasation Injury from the Anthracycline Antibiotics
Volume: 13 Issue: 10
Author(s): James H. Doroshow
Affiliation:
Keywords: Dexrazoxane, anthracycline, doxorubicin, oxidative stress, iron, chelator, cardiac toxicity, extravasation injury, cumulative cardiac toxicity, antineoplastic activity, oxygen species, tissue necrosis, daunorubicin, non-Hodgkin’s lymphoma, tissue injury.
Abstract: The cumulative cardiac toxicity of the anthracycline antibiotics and their propensity to produce severe tissue injury following extravasation from a peripheral vein during intravenous administration remain significant problems in clinical oncologic practice. Understanding of the free radical metabolism of these drugs and their interactions with iron proteins led to the development of dexrazoxane, an analogue of EDTA with intrinsic antineoplastic activity as well as strong iron binding properties, as both a prospective cardioprotective therapy for patients receiving anthracyclines and as an effective treatment for anthracycline extravasations. In this review, the molecular mechanisms by which the anthracyclines generate reactive oxygen species and interact with intracellular iron are examined to understand the cardioprotective mechanism of action of dexrazoxane and its ability to protect the subcutaneous tissues from anthracycline-induced tissue necrosis.
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Cite this article as:
H. Doroshow James, Dexrazoxane for the Prevention of Cardiac Toxicity and Treatment of Extravasation Injury from the Anthracycline Antibiotics, Current Pharmaceutical Biotechnology 2012; 13 (10) . https://dx.doi.org/10.2174/138920112802273245
DOI https://dx.doi.org/10.2174/138920112802273245 |
Print ISSN 1389-2010 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4316 |
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