Carrera Puerta, Esther

An indirect enzyme-linked immunosorbent assay (ELISA) has been developed for the identification of albacore (Thunnus alalunga) and its differentiation from other lessvalued scombrid species such as yellowfin tuna (Thunnus albacares), bullet tuna (Auxis rochei), atlantic bonito (Sarda sarda), bigeye tuna (Thunnus obesus), little tunny (Euthynnus alleteratus) and skipjack tuna (Katsuwonus pelamis). The assay uses polyclonal antibodies raised in rabbits against soluble muscle protein extract from fresh albacore. These polyclonal antibodies were rendered species-specific by blocking them with the heterologous soluble muscle proteins, allowing discrimination between fresh albacore and the rest of the scombrid species, except for yellowfin tuna. A total of 40 commercial albacore fresh and frozen fillets were analysed, revealing an incorrect labelling in 32.5% of the albacore samples. However, positive samples (67.5%) could be albacore or yellowfin tuna and should require a DNA assay as discriminatory technique.

Oxidative stress, defined as the excess production of reactive oxygen species (ROS) relative to antioxidant defense, plays a significant role in the development of cardiovascular diseases. Endoplasmic reticulum (ER) stress has emerged as an important source of ROS and its modulation could be cardioprotective. Previously, we demonstrated that miR-16-5p is enriched in the plasma of ischemic dilated cardiomyopathy (ICM) patients and promotes ER stress-induced apoptosis in cardiomyocytes in vitro. Here, we hypothesize that miR-16-5p might contribute to oxidative stress through ER stress induction and that targeting miR-16-5p may exert a cardioprotective role in ER stress-mediated cardiac injury. Analysis of oxidative markers in the plasma of ICM patients demonstrates that oxidative stress is associated with ICM. Moreover, we confirm that miR-16-5p overexpression promotes oxidative stress in AC16 cardiomyoblasts. We also find that, in response to tunicamycin-induced ER stress, miR-16-5p suppression decreases apoptosis, inflammation and cardiac damage via activating the ATF6-mediated cytoprotective pathway. Finally, ATF6 is identified as a direct target gene of miR-16-5p by dual-luciferase reporter assays. Our results indicate that miR-16-5p promotes ER stress and oxidative stress in cardiac cells through regulating ATF6, suggesting that the inhibition of miR-16-5p has potential as a therapeutic approach to protect the heart against ER and oxidative stress-induced injury.

La política europea de seguridad alimentaria tiene como objetivo garantizar a los ciudadanos una alimentación segura y nutritiva, basada en el análisis del riesgo, compuesto por la determinación del riesgo (asesoramiento científico y análisis de datos), gestión del riesgo (reglamentación y control) y comunicación sobre el riesgo. La sociedad presente y futura plantea retos sociales y sanitarios que pueden comprometer el nivel de seguridad alimentaria, como la globalización, aparición de nuevos alimentos y riesgos emergentes, realización de la compra online, etc., haciendo imprescindible el control por parte de las autoridades sanitarias, así como el autocontrol de los operadores alimentarios, la prevención y el enfoque global, y el compromiso de todos los sectores involucrados (productivo, transformador y comercial). En este capítulo, se abordan fortalezas y debilidades características del grupo poblacional de las personas mayores que, dado el contexto actual y futuro, pueden vulnerar la seguridad alimentaria y la salud de éstos. Asimismo, se muestran posibles amenazas, oportunidades y recomendaciones para evitarlas.

Congenital malformations are a common adverse outcome in pregnancies complicated by pregestational obesity, although the underlying mechanisms are still unrevealed. Our aim was to study the effect of oxidative stress in obesity-induced teratogenesis. Wistar rats were fed a high-fat diet for 13 weeks, with (OE group) or without (O group) vitamin E supplementation. Then, rats were mated and sacrificed at day 11.5 of gestation. Embryos from O dams presented a 25.9 3.5% rate of malformations (vs. 8.7 3.4% in C rats), which was reduced in the OE group (11.5 2.3%). Pregestational obesity induced hepatic protein and DNA oxidation and a decline in antioxidant enzymes. Importantly, glutathione content was also decreased, limiting the availability of this antioxidant in the embryos. Vitamin E supplementation efficiently maintained glutathione levels in the obese mothers, which could be used in their embryos to prevent oxidation-induced malformations. To test the effect of decreasing glutathione levels alone in a cell culture model of neuroepithelium, murine embryonic stem cells (ESC) were induced to form neuronal precursors and glutathione synthesis was inhibited with the gamma–glutamylcysteine synthesis inhibitor, buthionine sulfoximine (BSO). BSO inhibited the expression of Pax3, a gene required for neural tube closure that is also inhibited by oxidative stress. Taken together, our data indicate that obesity causes malformations through the depletion of maternal glutathione, thereby decreasing glutathione-dependent free radical scavenging in embryos, which can be prevented by vitamin E supplementation.