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Division of Applied Pharmacological Research, Food and Drug Administration (HFD-910), Laurel, Maryland 20908 [E. H. H., J. Z.]; Division of Pediatric Cardiology, School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York 14642 [S. E. L.]; Department of Laboratory Medicine, Children's Hospital, Boston, Massachusetts 02115 [N. R.]; Division of Cardiorenal Drug Products, Food and Drug Administration, (HFD-110), Rockville, Maryland 20852 [T. P.]; and Pathology Section, National Heart, Lung and Blood Institute, NIH, Bethesda, Maryland 20892 [Z-X. Y., K. T., V. J. F.]
The release of cardiac troponin T (cTnT) as a biomarker of doxorubicin-induced chronic cardiac injury was evaluated in the spontaneously hypertensive rat (SHR) model. Elevations in serum levels of cTnT and decreased immunohistochemical staining of heart sections for this protein were noted in SHRs treated with cumulative doses of doxorubicin (7 mg/kg) that induced only minimal histological alterations in myocytes. Concentrations of cTnT were further elevated, coincident with reduced immunohistochemical staining, in SHRs given 10–12 mg/kg doxorubicin.
Thus, monitoring serum levels of cTnT can detect doxorubicin-induced myocyte damage in SHR and may prove useful for the noninvasive evaluation of this toxicity in humans.
1 To whom requests for reprints should be addressed, at Division of Applied Pharmacological Research (HFD-910), Center for Drug Evaluation and Research, Food and Drug Administration, 8301 Muirkirk Road, Laurel, MD 20708. Phone: (301) 594-6020; Fax: (301) 594-3037
Received 9/15/97. Accepted 12/ 1/97.
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