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DNA damage and nitric oxide synthesis in experimentally infected Balb/c mice with Trypanosoma cruzi
Daniel A Ribeiro1, Sueli A Calvi, Mariele M Picka
1Department Health Sciences, Federal University of Sao Paulo, UNIFESP, SP, Brazil. daribeiro@unifesp.br
Abstract:
This study aimed to evaluate whether experimental Chagas disease in acute phase under benznidazole therapy can cause DNA damage in peripheral blood, liver, heart, and spleen cells or induce nitric oxide synthesis in spleen cells. Twenty Balb/c mice were distributed into four groups: control (non-infected animals); Trypanosoma cruzi infected; T. cruzi infected and submitted to benznidazole therapy; and only treated with benznidazole. The results obtained with the single cell gel (comet) assay showed that T. cruzi was able induce DNA damage in heart cells of both benznidazole treated or untreated infected mice. Similarly, T. cruzi infected animals showed an increase of DNA lesions in spleen cells. Regarding nitric oxide synthesis, statistically significant differences (p<0.05) were observed in all experimental groups compared to negative control, the strongest effect observed in the T. cruzi infected group. Taken together, these results indicate that T. cruzi may increase the level of DNA damage in mice heart and spleen cells. Probably, nitric oxide plays an important role in DNA damaging whereas benznidazole was able to minimize induced T. cruzi genotoxic effects in spleen cells.
Insights
Experimental Chagas disease causes DNA damage in mice heart and spleen cells, likely via nitric oxide. Benznidazole therapy partially reduced these genotoxic effects in spleen cells.
Area of Science:
- Parasitology
- Molecular Biology
- Toxicology
Background:
- Chagas disease, caused by Trypanosoma cruzi, is a significant global health concern.
- Understanding the genotoxic effects of T. cruzi infection and the protective role of benznidazole is crucial for treatment strategies.
Purpose of the Study:
- To investigate DNA damage in various organs of mice with experimental Chagas disease.
- To assess the impact of benznidazole therapy on T. cruzi-induced genotoxicity.
- To explore the role of nitric oxide synthesis in Chagas disease-associated DNA damage.
Main Methods:
- Experimental infection of Balb/c mice with Trypanosoma cruzi.
- Administration of benznidazole therapy to infected mice.
- Evaluation of DNA damage using the single cell gel (comet) assay.
- Measurement of nitric oxide synthesis in spleen cells.
Main Results:
- Trypanosoma cruzi infection induced DNA damage in heart and spleen cells.
- Increased DNA lesions were observed in spleen cells of infected mice.
- Nitric oxide synthesis was significantly elevated in infected mice, particularly in the T. cruzi infected group.
- Benznidazole therapy showed a protective effect, minimizing T. cruzi-induced genotoxicity in spleen cells.
Conclusions:
- Trypanosoma cruzi infection can lead to increased DNA damage in mice heart and spleen.
- Nitric oxide likely plays a role in the DNA damaging effects of T. cruzi.
- Benznidazole therapy demonstrates potential in mitigating the genotoxic impact of Chagas disease in spleen cells.
