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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Genotoxicity assessment of the antimalarial compound artesunate in somatic cells of mice

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Author(s):
Aquino, Ivani [1] ; Perazzo, Fabio Ferreira [2] ; Maistro, Edson Luis [3]
Total Authors: 3
Affiliation:
[1] Univ Estadual Paulista, UNESP, Inst Biociencias, Programa Posgrad Biol Geral & Aplicada, BR-18618970 Botucatu, SP - Brazil
[2] Univ Fed Sao Paulo UNIFESP, Dept Ciencias Exatas & Terra, BR-09972270 Diadema, SP - Brazil
[3] Univ Estadual Paulista, UNESP, Fac Filosofia & Ciencias, Dept Fonoaudiol, BR-17525900 Marilia, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Food and Chemical Toxicology; v. 49, n. 6, p. 1335-1339, JUN 2011.
Web of Science Citations: 16
Abstract

Artesunate is a derivate of artemisinin that is both an antimalarial agent and acts cytotoxically on tumor cells. Despite its therapeutic use, its in vivo genotoxic potential has still not been evaluated. This study, therefore, was an investigation into the effects of a single oral administration of artesunate with an in vivo comet assay that analyzed leukocytes from peripheral blood and liver cells, and a micronucleus (MN) assay of bone marrow cells from male Swiss mice. The artesunate was administered by oral gavage at doses of 5, 50 and 100 mg/kg. Cytotoxicity was assessed by scoring 200 consecutive polychromatic (PCE) and normochromatic (NCE) erythrocytes (PCE/NCE ratio). The results demonstrate that artesunate induced significant DNA damage only in liver cells and that high doses of artesunate caused an increase in the mean number of micronucleated polychromatic erythrocytes (MNPCE). Under our experimental conditions, artesunate showed weak genotoxic effects at low doses and clastogenic effects at high doses. The PCE/NCE ratio indicated no cytotoxicity. The data obtained suggest caution about either continuous or high-dose use of artesunate by humans. (C) 2011 Elsevier Ltd. All rights reserved. (AU)