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BioMed Research International
Volume 2014, Article ID 580626, 9 pages
http://dx.doi.org/10.1155/2014/580626
Research Article

Oral and Intraperitoneal Administration of Quercetin Decreased Lymphocyte DNA Damage and Plasma Lipid Peroxidation Induced by TSA In Vivo

1Department of Nutritional Science, Chung Shan Medical University, No. 110 Section Jianguo North Road, Taichung 40201, Taiwan
2Department of Nutrition, Hungkuang University, No. 34 Chung Chie Road, Shalu, Taichung County 43302, Taiwan
3Department of Beauty Science, Chienkuo Technology University, Changhua 50094, Taiwan
4Graduate Institute of Veterinary Pathology, College of Veterinary Medicine, National Chung Hsing University, Taichung 40227, Taiwan
5Department of Nutrition, Chung Shan Medical University Hospital, Taichung 40201, Taiwan

Received 23 December 2013; Accepted 27 March 2014; Published 23 April 2014

Academic Editor: Chia-Chien Hsieh

Copyright © 2014 Shu-Ting Chan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Our previous study showed that quercetin enhances the anticancer effect of trichostatin A (TSA) in xenograft mice given quercetin intraperitoneally (10 mg/kg, 3 times/week). Herein, we investigate whether quercetin administered orally exerts such an effect and prevents the cytotoxic side effects of TSA. We found that quercetin given orally (20 and 100 mg/kg, 3 times/week) failed to enhance the antitumor effect of TSA although it increased the total quercetin concentration more than quercetin administered intraperitoneally in the plasma. The compound quercetin-3-glucuronide (Q3G) increased the most. However, quercetin administered intraperitoneally increased the total quercetin level in tumor tissues more than oral quercetin. Oral and intraperitoneal administration of quercetin similarly decreased lymphocyte DNA damage and plasma lipid peroxidation level induced by TSA. Furthermore, we found that the enhancing effect of Q3G on the antitumor effect of TSA and the incorporation of Q3G was less than that of quercetin in A549 cells. However, we found that A549 cells possessed the ability to convert Q3G to quercetin. In conclusion, different from quercetin administered intraperitoneally, quercetin administered orally failed to enhance the antitumor effect of TSA because of its metabolic conversion. However, it prevented TSA-induced DNA damage and lipid peroxidation.