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Potentiation of Doxorubicin cardiotoxicity by iron loading in a rodent model.

Abstract：

OBJECTIVES:The role of iron toward doxorubicin (DOX) cardiotoxicity was studied using a rodent model of dietary carbonyl iron loading. BACKGROUND:Doxorubicin, a commonly used anticancer drug, is known to cause serious and potentially life-threatening cardiotoxicity. Doxorubicin cardiotoxicity is thought to be mediated through free-radical injury. METHODS:Male Sprague Dawley rats fed iron-rich chow (n = 8) and regular chow (n = 8) were treated with DOX or saline (4 animals in each arm). Cardiotoxicity was assessed using mortality, weight changes, Tc-99m annexin-V imaging, histopathology, and immunohistochemistry. RESULTS:Animals fed iron-rich chow showed significantly higher DOX cardiotoxicity as evidenced by greater weight loss (107 +/- 14 g vs. 55 +/- 10 g weight loss, p < 0.05), higher annexin uptake (0.14 +/- 0.01% vs. 0.08 +/- 0.01% injected dose/g of myocardium, p < 0.05), more severe myocyte injury on electron microscopy, and significantly higher cleaved caspase-3 staining compared with regular chow fed rats given DOX. Feeding iron-rich chow alone did not result in any cardiotoxicity. CONCLUSIONS:Dietary iron loading resulted in a substantially increased DOX cardiotoxicity in rats. Body iron stores as well as its bioavailability in tissue may be important independent predictors of susceptibility to DOX cardiotoxicity in man. Further clinical studies are warranted.

journal_name

J Am Coll Cardiol

journal_title

Journal of the American College of Cardiology

authors

Panjrath GS,Patel V,Valdiviezo CI,Narula N,Narula J,Jain D

doi

10.1016/j.jacc.2007.02.060

subject

Has Abstract

pub_date

2007-06-26 00:00:00

pages

2457-64

issue

25

eissn

0735-1097

issn

1558-3597

pii

S0735-1097(07)01221-1

journal_volume

49

pub_type

杂志文章

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