RESUMENLas hojas de la planta Xanthium spinosum se utilizan culturalmente en Paraguay por sus propiedades medicinales. Se evaluó la toxicidad aguda del extracto de hojas maduras; para el estudio se seleccionaron 35 ratones BALB/C machos que fueron distribuidos en 7 grupos, 6 de ensayo y 1 de control. El extracto fue preparado en concentraciones de 6 y 9% (g/dL); se administró la solución 6% a tres grupos y la solución 9% a los otros tres grupos, con dosis entre 200 y 1000 mg/kg. Al final de 14 días de observación, se extrajeron muestras de sangre para estudios laboratoriales de urea y transaminasas, además de órganos para estudios anatomopatológicos. Se determinaron aumentos en los niveles de GOT y urea en comparación al grupo control. Se concluye que el consumo del extracto de hojas maduras de Xanthium spinosum puede causar daño hepático.Palabras clave: Xanthium spinosum; Toxicidad aguda; Plantas medicinales (fuente: DeCS BIREME). ABSTRACTThe leaves of the Xanthium spinosum plant have been used culturally in Paraguay for their medicinal properties. Acute toxicity of mature leaf extract was evaluated. For the study, 35 Balb/c mice were selected and allocated into 7 groups, 6 test groups and 1 control group. The extract was prepared in concentrations of 6% and 9% (g/dL). The 6% concentration was administrated to 3 test groups and 9% concentration to the remaining 3 groups, with doses between 200 and 1000 mg/kg per mouse. After 14 days of observation, blood samples were taken for laboratory studies of urea and transaminases and organs were examined for pathological studies. There were increased levels of GOT and urea in the test groups compared to the control group. In conclusion, the consumption of mature leaf extract of Xanthium spinosum can cause hepatic damage.

Chagas disease is a potentially fatal disease caused by the parasite Trypanosoma cruzi, which can in some cases affect the central nervous system. The objective was to evaluate the effect of aspirin (ASA) in the behavior of mice infected with T. cruzi during the acute phase. This was an experimental study with random assignation. Twenty four BALB/c mice were divided into four groups of six animals each as follows: only ASA (OA), ASA before infection (BI), ASA after infection (AI) and only infection (OI). The strain used for infection was M/HOM/Bra/53/Y. An ASA dose of 100 mg/kg per day was administered 72 h before infection to BI group and the same dose 48 h after infection to AI group. Mice behavior in the open field test, mortality, and brain histopathology was evaluated. Data were analyzed using ANOVA, chi square test, and Kaplan-Meier with long-rank for survival analysis. In the open field test, the OA group has similar results with the BI group, in the variables of immobility and escape. Also, the OA group displayed significantly higher rates of micturition (p < 0.001) and defecation (p < 0.001) compared to infected groups. Mortality was higher in BI group (p = 0.02). The presence of T. cruzi amastigotes were higher in brain tissues of the AI and OI groups (p = 0.008). In conclusion, the administration of ASA before infection seemed to prevent behavioral changes induced by the acute infection, but it led to accelerated mortality. The study highlighted the potential importance of the pathways inhibited by ASA in the early hours of acute infection with T. cruzi.

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