DNA damage and nitric oxide production in mice following infection with L. chagasi
Mutation Research-genetic Toxicology and Environmental Mutagenesis. Amsterdam: Elsevier B.V., v. 723, n. 2, p. 177-181, 2011.
Cardoso de Oliveira, Larissa Ragozo
Gomes Cezario, Glaucia Aparecida
Goncalves de Lima, Carlos Roberto
Nicolete, Vanessa Cristina
de Sibio, Maria Tereza
Modolo Picka, Mariele Cristina
Calvi, Sueli Aparecida
Leishmania chagasi, which causes visceral leishmaniasis in South America, is an obligate intracellular protozoan. Production of nitric oxide by macrophages during the inflammatory response is one of the main microbicidal mechanisms against this parasite. The goal of this study was to evaluate whether L. chagasi infection causes DNA damage in peripheral blood and spleen cells of Balb/c mice and whether such damage may be related to NO production. Balb/c mice were either infected with L chagasi or maintained as controls. The single-cell gel electrophoresis (comet) assay was used to measure DNA damage in peripheral blood and spleen cells, and the Griess reaction was used to measure NO production in the spleen. L chagasi infection induced DNA damage in peripheral blood and spleen cells of infected mice. Macrophages from the control group, challenged with L. chagasi, showed significantly (p < 0.05) greater NO production, compared to non-challenged cells. Treatment of spleen cells with N(G)-monomethyl-L-arginine (LNMMA) caused a significant reduction of NO production and DNA damage (p < 0.05). Our results indicate that L. chagasi induces DNA damage in the peripheral blood and spleen cells and that NO not only causes killing of the parasite but also induces DNA damage in adjacent cells. (C) 2011 Elsevier B.V. All rights reserved.