It has been proposed that oxidative stress is a pathogenic mechanism to induce cytotoxicity and to cause cardiovascular and neuronal diseases. At present, natural compounds such as plant extracts have been used to reduce the cytotoxic effects produced by agents that induce oxidative stress. Our study aimed to evaluate the antioxidant and cytoprotective capacity of Desmodium tortuosum (D. tortuosum) extract in the co- and pre-treatment in EA.hy926 and SH-SY5Y cell lines subjected to oxidative stress induced by tert-butylhydroperoxide (t-BOOH). Cell viability, reactive oxygen species (ROS), nitric oxide (NO), caspase 3/7 activity, reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), and molecular expression of oxidative stress biomarkers (SOD2, NRF2 and NFκB1) and cell death (APAF1, BAX, Caspase3) were all evaluated. It was observed that the D. tortuosum extract, in a dose-dependent manner, was able to reduce the oxidative and cytotoxicity effects induced by t-BOOH, even normalized to a dose of 200 µg/mL, which would be due to the high content of phenolic compounds mainly phenolic acids, flavonoids, carotenoids and other antioxidant compounds. Finally, these results are indicators that the extract of D. tortuosum could be a natural alternative against the cytotoxic exposure to stressful and cytotoxic chemical agents.

This study aimed to investigate the toxicity of the fungicide ipconazole on oxidative status, cell death and inflammasome complex activation in the hypothalamus, cerebral cortex, striatum and hippocampus of rats. Female albino rats were randomly divided into a control group and four groups treated with ipconazole at doses of 1, 5, 10 and 20 mg/kg b.w., administered for six days. Ipconazole significantly increased MDA and ROS levels in all brain regions studied, while reducing catalase enzyme activity. The molecular expression of cell death-related genes (AKT1, APAF1, BNIP3, CASP3 and BAX) and the inflammasome complex (CASP1, IL1β, IL6, NLRP3, NFĸB and TNFα) was also assessed, showing increased expression in at least one brain region. The findings demonstrate that ipconazole induces central nervous system toxicity in mammals, highlighting its potential role as a risk factor in the development of neurodegenerative disorders in individuals exposed to this contaminant.

Brunfelsia grandiflora is a South American solanaceae widely used since long ago for its recognized medicinal properties. We have recently reported its chemical composition, showing a relevant number of bioactive compounds with antioxidant capacity, and proved the cytoprotective and antioxidative stress potential of B. grandiflora in cultured endothelial cells. Since B. grandiflora extracts have shown effects on the central nervous system, the present study was designed to show the potential cytoprotective capacity and the antioxidative stress potential of phenolic extracts from the plant on cultured neuron-like cells, as a model to reduce the presentation or effects of chronic diseases of the nervous system. To this end, we studied its reactive oxygen species (ROS)-reducing capacity, its antioxidant defense mechanisms, and some molecular markers involved in redox balance and apoptosis. The results show that cell survival and most changes in biomarkers related to oxidative status, ROS, reduced glutathione, glutathione peroxidase and reductase, malondialdehyde, and caspase 3/7 activity, and molecular expression of cell death-related genes (BAX, BNIP3, and APAF1), NFκB, SOD, and NRF2 (genes from oxidative stress—antioxidants) induced by oxidative stress were prevented by either co- or pretreatment of neuron-like cells with B. grandiflora extracts (25–200 µg/mL). The results demonstrate the chemoprotective potential of the plant and support its medicinal use.

In developing countries, river monitoring is very limited. Despite environmental and health problems, there is a paucity of information regarding the contaminants phosphates and nitrates. Thus, concentration and health risks, of phosphates and nitrates of the Ichu river waters, in Huancavelica,...

El uso y abuso de etanol es asociado frecuentemente con implicaciones y consecuencias medicolegales. El objetivo de este estudio fue evaluar la alcoholemia retrospectiva en función de dos muestras sanguíneas sucesivas de personas con posingestión de bebidas alcohólicas. El etanol como cerveza se administró en dosis única 0,8 g/kg a los sujetos del grupo I, se recogió cantidad suficiente de muestras de sangre diseñándose el perfil de concentración-tiempo del etanol y determinaron parámetros toxicocinéticos; los grupos II, y III libaron cerveza ad libitum y se extrajeron dos muestras de sangre a diferentes intervalos de tiempo. El etanol se cuantificó por cromatografía de gases. Las extrapolaciones retrógradas de alcoholemias se estimaron suponiendo cinética de orden cero y rango de tasas de eliminación 0,10 a 0,35 g/L/h. En el grupo I se determinó el volumen de distribución 0,70 L/kg, alcoholemia máxima 1,05 g/L a los 60 min y 0,148 g/L/h la tasa promedio de eliminación. Se demostró que solo en el grupo III los promedios de las concentraciones de etanol en la segunda muestra de sangre fueron menores que la primera, significando fase de eliminación y los datos de alcoholemia retrospectiva con límites superior e inferior fueron precisos, viables y válidos. En conclusión, los niveles de alcoholemia de una persona obtenidas en dos muestras de sangre con separación de 30 a 45 min, la primera extraída inmediatamente ocurrido el hecho punible y en fase de eliminación permiten la estimación de los límites superior e inferior de alcoholemia retrospectiva con precisión y alta fiabilidad frente al estudio tradicional de alcoholemia con solo una muestra de sangre.