ORIGINAL PAPER Selenium supplementation at low doses contributes to the decrease in heart damage in experimental Trypanosoma cruzi infection Received: 21 November 2002 / Accepted: 9 January 2003 / Published online: 22 July 2003 Ó Springer-Verlag 2003 Abstract Chagasic patients with cardiomyopathy have low levels of selenium (Se), a fundamental trace element. We evaluated the effect of supplementing infected mice with Se (0.25–16 ppm). Supplementation with 0.25 or 1 ppm Se led to parasitaemia and survival curves similar to those of the control group. Mice treated with 4– 16 ppm showed a dose-dependent decrease of parasita- emia, significant for the highest concentration. This was probably due to a direct effect on the parasites, which were lysed after in vitro incubation with Se. Survival rates did not change significantly; however, heart dam- age was reduced in infected mice supplemented with 4 ppm Se, as indicated by a lower cardiac isoform of creatine kinase levels. Our results imply that Se supple- mentation does not lead to a general protection during infection, but may help protect the heart from inflam- matory damage. The effect of Se supplementation in the course of T. cruzi infection depends on the host-parasite pair employed. Introduction Selenium (Se) is a fundamental trace element to organisms from bacteria to humans that has an important metabolic role since it is incorporated into Se-dependent enzymes such as glutathione peroxidase, which is involved in protection against oxidative stress (Barceloux 1999). Adequate Se nourishment decreases the risk of cancer, cardiovascular diseases and neuro- degenerative disorders (Ganther 1999; Ne` ve 2000; Raich et al. 2001). Diet complementation with Se could then be beneficial in the treatment of diseases corre- lated with high levels of oxidative stress (Hennet et al. 1992; Taylor et al. 2000). Chagas’ disease, caused by Trypanosoma cruzi, is an important cause of myocardiopathy in Latin America, leading to great morbidity and mortality. Malnutrition also affects populations from endemic areas, but studies regarding its impact on the course of human infection are scarce (Andrade and Zincker 1995). We have shown a reduction of Se levels in chronic chagasic patients with ongoing active myocardiopathy (Rivera et al. 2002), and an enhancement of susceptibility to experimental T. cruzi infection in mice fed with Se-deficient food (De Souza et al. 2002). A recent paper by Gomez et al. (2002), using a similar strategy for experimentally reducing Se plasma levels, also contributed to the con- cept that a decrease in Se is associated with a greater pathological effect. The immediate hypothesis opened by these results is that exogeneous supplementation with Se would be beneficial to chagasic patients or T. cruzi-infected animals. In the sole paper on Se supplementation and Chagas’ disease, Davis et al. (1998) reported that sodium selenate, added to the drinking water, decreased both the parasitaemia and mortality of C3H mice infected with the Brazil strain of T. cruzi. Since the course of infection presents different profiles depending on the model used (Arau´ jo-Jorge 2000), we decided to further address this question. We used outbred Swiss mice infected with the highly virulent Y strain of T. cruzi and evaluated parasitaemia, mor- tality and the corresponding heart damage, which was indirectly indicated by the cardiac isoform of creatine kinase levels (CK-MB) as previously described (De Souza et al. 2000; Henriques-Pons et al. 2002). Parasitol Res (2003) 91: 51–54 DOI 10.1007/s00436-003-0867-9 Andre´a P. de Souza Æ Gabriel Melo de Oliveira Jean Vanderpas Æ Solange L. de Castro Maria Teresa Rivera Æ Tania C. Arau´jo-Jorge A. P. de Souza Æ G. M. de Oliveira Æ S. L. de Castro M. T. Rivera Æ T. C. Arau´jo-Jorge (&) Laborato´rio de Biologia Celular, Departamento de Ultra-estrutura e Biologia Celular, Instituto Oswaldo Cruz, Fundac¸a˜o Oswaldo Cruz, Av. Brasil 4365, Manguinhos, 21045-900 Rio de Janeiro, RJ, Brazil E-mail: taniaaj@ioc.fiocruz.br Tel.: +55-21-5984332 Fax: +55-21-2604434 J. Vanderpas Hoˆpital Ambroise-Pare´, Bv. Kennedy 2, 7000 Mons, Belgium