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Several studies demonstrated the toxicity of aspartame (ASP) and aflatoxin B1 (AFB1 ) in preclinical models. Although the majority of these reports assessed the toxic effects of each substance separately, their concomitant exposure and hazardous consequences are scarce. Importantly, the deleterious effects at the central nervous system caused by ASP and AFB1 co-exposure are rarely addressed. We evaluated if concomitant exposure to AFB1 and ASP would cause behavioral impairment and alteration in oxidative status of the brain in male rats. Animals received once a day for 14 days AFB1 (250 µg/kg, intragastric gavage [i.g.]), ASP (75 mg/kg, i.g.), or both substances (association). On day 14, they were subjected to behavioral evaluation, and biochemical and molecular parameters of oxidative status were measured in the cerebral cortex and hippocampus. In the open field test, AFB1 and combination treatments modified the motor, exploratory, and grooming behavior. In the splash test, all treatments caused a reduction in grooming time compared to the control group. An increase in thiobarbituric acid-reactive substances content induced by AFB1 and combination treatments was observed. The antioxidant defenses (vitamin C, nonprotein sulfhydryl, and ferric reducing antioxidant power) were impaired in all groups compared to control. Regarding molecular evaluation, mitochondrial superoxide dismutase-2 immunoreactivity decreased after AFB1 or ASP exposition in the hippocampus. Thus, co-exposure to ASP and AFB1 was potentially more toxic because it aggravated behavioral impairments and oxidative status disbalance in comparison to the groups that received only ASP or AFB1 . Therefore, our data suggest that those substances caused a disruption in brain homeostasis.

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The potential interactions among food additives/contaminants and the consequences to biological systems is a topic that is rarely addressed in scientific literature. Thus, the current study investigated if the combined administration of ASP and AFB1 would impair hepatic and renal oxidative status. Male Wistar rats received during 14 days once a day ASP (75 mg/Kg) and/or AFB1 (250 µg/Kg) through intragastric route. At the end of experimental protocol, samples of liver and kidneys were collected for assessing biochemical markers of oxidative status. In the hepatic tissue, the treatment with a single substance (ASP or AFB1) caused an increase in TBARS levels, and a reduction in non-enzymatic antioxidant defenses (Vit C and NPSH levels and FRAP test). In the kidneys, TBARS levels were increased only in the group that received ASP + AFB1. The association reduced NPSH content, while the treatment with AFB1 reduced the FRAP levels. GST and CAT activities were increased in all treatments. Overall, ASP and AFB1 association presented higher toxic effects to the tissues. To the best of our knowledge, this is the first study demonstrating that the associated use of both ASP and AFB1 induces more extensive injuries in comparison to the effects caused by each one alone. Therefore, these data demonstrated that concomitant exposure to ASP and AFB1 potentiated their oxidative damage in hepatic tissue, suggesting that this organ is particularly sensitive to the toxic action induced by these substances.

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Artificial sweeteners are mainly used as substitutes for sucrose derivates. In this study, we analyzed if the chronic consumption of aspartame or acesulfame potassium at an early age, produces histological alterations, astrogliosis and decreased neuronal viability, in hippocampus, prefrontal cortex, amygdala and hypothalamus of male Wistar rats. A histological analysis was performed on male Wistar rats that consumed aspartame or acesulfame potassium during 90 days, initiating the consumption of sweeteners immediately after weaning. The evaluation of neuronal morphology in different areas of the brain was performed with hematoxylin - eosin staining. To measure astrogliosis and neuronal viability, we used the immunohistochemical technique, with the glial fibrillary acidic protein immunomodulators (GFAP) and with neuronal-specific enolase (NSE). The consumption of aspartame or acesulfame potassium promoted morphological changes of neurons including increased pyknotic nuclei and vacuolization in all the brain areas studied. In hippocampus, prefrontal cortex, amygdala and hypothalamus, astrogliosis and reduction of neural viability were observed in sweeteners consumers in comparison with the control group. Chronic consumption of ASP and ACK from early stages of development and during long periods, may promote neural modifications, astrogliosis and decrease neuronal viability in prefrontal cortex, amygdala, hippocampus, and hypothalamus.

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Aspartame is a synthetic sweetener consumed by more than half the adult population in 75 countries. Their metabolites can be toxic, principally to the liver and retina, and there are few studies on the use of aspartame in gestation. Twenty pregnant rats were weighed and allocated randomly (n=5 per group) to receive 14 mg/kg aspartame or water by oral-gastric drip. Treated Tl: aspartame diluted in water at room temperature; Treated T2: aspartame diluted in water heated to 40° C; control Cl: water at room temperature; and control C2: water heated to 40° C. Placentas were weighed, umbilical cords measured and 1000 nuclei of fetal hepatocytes (250 from each group) were analyzed morphometrically utilizing the technique of kariometry, with application of the Mann-Whitney U-Test. There were reductions in mean placental and maternal-fetal weights, in umbilical-cord length, and the majority of kariometric parameters of the hepatocytes in the group treated with aspartame diluted in distilled water at room temperature. Reduction of placental and maternal-fetal weights occurred, shortening of the umbilical cord, and decrease in kariometric parameters in fetal hepatocyte nuclei after administration of aspartame diluted in distilled water at 40°C temperature. The use of aspartame during gestation can be prejudicial to the fetus.

El aspartame es un endulzante sintético consumido por más de la mitad de la población adulta, en 75 países. Sus metabolitos pueden ser tóxicos, principalmente en el hígado y retina y hay algunos estudios sobre el aspartame en el embarazo. Veinte ratas preñadas fueron pesadas y distribuidas aleatoriamente (n=5 por grupo) y recibieron 14 mg/Kg de aspartame o agua por vía oral- gástrica. Tratamiento 1: aspartame diluido en agua a temperatura ambiente; Tratamiento T2: aspartame diluido en agua tibia a 40 °C; control Cl: agua a temperatura ambiente, y control C2: agua tibia a 40° C. Las placentas fueron pesadas, el cordón umbilical medido y 1000 núcleos de hepatocitos fetales (250 de cada grupo) se analizaron morfométricamente utilizando la técnica de canometría con aplicación del Test U de Mann-Whitney U-Test. En el grupo tratado con aspartame diluido en agua a temperatura ambiente, hubo reducción en los pesos promedios de la placenta y materno-fetal, largo del cordón umbilical y en la mayoría de los parámetros cartométricos de los hepatocitos. Lo mismo ocurrió en el grupo tratado con aspartame diluido en agua a 40 °C. El uso del aspartame durante las gestación puede ser perjudicial para el feto.

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El Aspartame es un potente edulcorante producido en forma sintética a partir del ácido aspártico y de la fenilanina. Es considerado como un edulcorante no calórico, por las pequeñas cantidades que se utilizan para obtener el sabor dulce deseado. El Aspartame es hidrolizado en el lumen intestinal y en las vellosidades de la mucosa y absorbido al estado de aspartato, fenilanina y metanol y también como el dipéptido aspartil-fenilanina. El edulcorante y los productos de su degradación no han demostrado toxicidad en el ser humano, aún a dosis muy superiores a las habitualmente empleadas. Sin embargo, no es recomendable el uso de Aspartame en niños portadores de fenilquetonuria, por las elevadas concentraciones sanguíneas de feneilanina que en ellos se puede alcanzar. El Aspartame puede ser consumido en forma segura por individuos obesos y pacientes diabéticos, por cuanto no modifica los niveles glicémicos, insulinémicos, glucagonémicos, ni interfiere con la hemoglobina glicosilada. Su uso está practicamente libre de efectos colaterales adverso

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