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Monohydroxyethylrutoside as protector against chronic doxorubicin-induced cardiotoxicity.
Br J Pharmacol 1995; 115(7):1260-4BJ

Abstract

1. The clinical use of the antitumour agent, doxorubicin, is largely limited by the development of a cumulative dose-related cardiotoxicity. This toxicity is generally believed to be caused by the formation of oxygen free radicals. In earlier studies it was established that flavonoids, naturally occurring antioxidants, can provide some degree of protection. In this study we investigated whether 7-monohydroxyethylrutoside (monoHER), a powerful antioxidative flavonoid with extremely low toxicity, can provide protection to an extent comparable to the clinically successful Cardioxane (ICRF-187). 2. Balb/c mice of 20-25 g were equipped i.p. with a telemeter to measure ECG. They were given 6 i.v. doses of doxorubicin (4 mg kg-1) at weekly intervals. ICRF-187 (50 mg kg-1) or monoHER (500 mg kg-1) were administered i.p. 1 h before doxorubicin administration. In the 2 monoHER groups the treatment continued with either 1 or 4 additional injections per week. A saline and monoHER treated group served as controls. After these 6 weeks, they were observed for another 2 weeks. 3. At the end of this study (week 8) the ST interval had increased by 16.7 +/- 2.7 ms (mean +/- s.e. mean) in doxorubicin-treated mice. At that time, the ST interval had increased by only 1.8 +/- 0.9 ms in ICRF-187 co-mediated mice and in monoHER co-medicated mice by only 1.7 +/- 0.8 and 5.1 +/- 1.7 ms (5- and 2-day schedule, respectively, all P < 0.001 relative to doxorubicin and not significantly different from control). The ECG of the control animals did not change during the entire study. The QRS complex did not change in either group.4. It can be concluded that monoHER protects against doxorubicin-induced cardiotoxicity and merits further evaluation in this respect.

Authors+Show Affiliations

LACDR, Department of Pharmacochemistry, Faculty of Chemistry, Vrije Universiteit, De Boelelaan, Amsterdam, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

7582554

Citation

van Acker, S A., et al. "Monohydroxyethylrutoside as Protector Against Chronic Doxorubicin-induced Cardiotoxicity." British Journal of Pharmacology, vol. 115, no. 7, 1995, pp. 1260-4.
van Acker SA, Kramer K, Grimbergen JA, et al. Monohydroxyethylrutoside as protector against chronic doxorubicin-induced cardiotoxicity. Br J Pharmacol. 1995;115(7):1260-4.
van Acker, S. A., Kramer, K., Grimbergen, J. A., van den Berg, D. J., van der Vijgh, W. J., & Bast, A. (1995). Monohydroxyethylrutoside as protector against chronic doxorubicin-induced cardiotoxicity. British Journal of Pharmacology, 115(7), pp. 1260-4.
van Acker SA, et al. Monohydroxyethylrutoside as Protector Against Chronic Doxorubicin-induced Cardiotoxicity. Br J Pharmacol. 1995;115(7):1260-4. PubMed PMID: 7582554.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Monohydroxyethylrutoside as protector against chronic doxorubicin-induced cardiotoxicity. AU - van Acker,S A, AU - Kramer,K, AU - Grimbergen,J A, AU - van den Berg,D J, AU - van der Vijgh,W J, AU - Bast,A, PY - 1995/8/1/pubmed PY - 1995/8/1/medline PY - 1995/8/1/entrez SP - 1260 EP - 4 JF - British journal of pharmacology JO - Br. J. Pharmacol. VL - 115 IS - 7 N2 - 1. The clinical use of the antitumour agent, doxorubicin, is largely limited by the development of a cumulative dose-related cardiotoxicity. This toxicity is generally believed to be caused by the formation of oxygen free radicals. In earlier studies it was established that flavonoids, naturally occurring antioxidants, can provide some degree of protection. In this study we investigated whether 7-monohydroxyethylrutoside (monoHER), a powerful antioxidative flavonoid with extremely low toxicity, can provide protection to an extent comparable to the clinically successful Cardioxane (ICRF-187). 2. Balb/c mice of 20-25 g were equipped i.p. with a telemeter to measure ECG. They were given 6 i.v. doses of doxorubicin (4 mg kg-1) at weekly intervals. ICRF-187 (50 mg kg-1) or monoHER (500 mg kg-1) were administered i.p. 1 h before doxorubicin administration. In the 2 monoHER groups the treatment continued with either 1 or 4 additional injections per week. A saline and monoHER treated group served as controls. After these 6 weeks, they were observed for another 2 weeks. 3. At the end of this study (week 8) the ST interval had increased by 16.7 +/- 2.7 ms (mean +/- s.e. mean) in doxorubicin-treated mice. At that time, the ST interval had increased by only 1.8 +/- 0.9 ms in ICRF-187 co-mediated mice and in monoHER co-medicated mice by only 1.7 +/- 0.8 and 5.1 +/- 1.7 ms (5- and 2-day schedule, respectively, all P < 0.001 relative to doxorubicin and not significantly different from control). The ECG of the control animals did not change during the entire study. The QRS complex did not change in either group.4. It can be concluded that monoHER protects against doxorubicin-induced cardiotoxicity and merits further evaluation in this respect. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/7582554/Monohydroxyethylrutoside_as_protector_against_chronic_doxorubicin_induced_cardiotoxicity_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&amp;sid=nlm:pubmed&amp;issn=0007-1188&amp;date=1995&amp;volume=115&amp;issue=7&amp;spage=1260 DB - PRIME DP - Unbound Medicine ER -