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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 874367, 7 pages
http://dx.doi.org/10.1155/2013/874367
Research Article

The Effects of N-Butyl-1-(4-dimethylamino)phenyl-1,2,3,4-tetrahydro-β-carboline-3-carboxamide against Leishmania amazonensis Are Mediated by Mitochondrial Dysfunction

1Programa de Pós-Graduação em Ciências Biológicas, Universidade Estadual de Maringá, Avenida Colombo 5790, PR 87020-900 Maringá, Brazil
2Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Avenida Colombo 5790, PR 87020-900 Maringá, Brazil
3Departamento de Química, Universidade Estadual de Maringá, Avenida Colombo 5790, PR 87020-900 Maringá, Brazil
4Programa de Pós-Graduação em Ciências Biológicas, Laboratório de Inovação Tecnológica no Desenvolvimento de Fármacos e Cosméticos, Bloco B-08, Universidade Estadual de Maringá, Avenida Colombo 5790, PR 87020-900 Maringá, Brazil

Received 21 January 2013; Accepted 27 May 2013

Academic Editor: Valdir Cechinel Filho

Copyright © 2013 Hélito Volpato 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

Leishmaniasis is a disease that affects millions of people worldwide. The drugs that are available for the treatment of this infection exhibit high toxicity and various side effects. Several studies have focused on the development of new chemotherapeutic agents that are less toxic and more effective against trypanosomatids. We investigated the effects of N-butyl-1-(4-dimethylamino)phenyl-1,2,3,4-tetrahydro- -carboline-3-carboxamide (C4) and its possible targets against L. amazonensis. The results showed morphological and ultrastructural alterations, depolarization of the mitochondrial membrane, the loss of cell membrane integrity, and an increase in the formation of mitochondrial superoxide anions in L. amazonensis treated with C4. Our results indicate that C4 is a selective antileishmanial agent, and its effects appear to be mediated by mitochondrial dysfunction.