Ribeiro Daniel A, Calvi Sueli A, Picka Mariele M, Persi Eliana, de Carvalho Thaís B, Caetano Priscila K, Nagoshi Lidiana R, Lima Carlos R G, Machado Jussara M, Salvadori Daisy M F
Department Health Sciences, Federal University of Sao Paulo, UNIFESP, SP, Brazil.
Exp Parasitol. 2007 Jul;116(3):296-301. doi: 10.1016/j.exppara.2006.12.007. Epub 2006 Dec 30.
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.
本研究旨在评估处于急性期的实验性恰加斯病在接受苯硝唑治疗的情况下，是否会导致外周血、肝脏、心脏和脾脏细胞的DNA损伤，或诱导脾脏细胞中的一氧化氮合成。将20只Balb/c小鼠分为四组：对照组（未感染动物）；克氏锥虫感染组；克氏锥虫感染并接受苯硝唑治疗组；仅接受苯硝唑治疗组。单细胞凝胶（彗星）试验结果表明，克氏锥虫能够在接受或未接受苯硝唑治疗的感染小鼠的心脏细胞中诱导DNA损伤。同样，克氏锥虫感染的动物脾脏细胞中的DNA损伤也有所增加。关于一氧化氮合成，与阴性对照组相比，所有实验组均观察到统计学上的显著差异（p<0.05），在克氏锥虫感染组中观察到的效应最强。综上所述，这些结果表明克氏锥虫可能会增加小鼠心脏和脾脏细胞中的DNA损伤水平。一氧化氮可能在DNA损伤中起重要作用，而苯硝唑能够将克氏锥虫诱导的脾脏细胞遗传毒性作用降至最低。
