RESUMEN Las úlceras por presión (UPP) y úlceras venosas (UV) son frecuentes en adultos y adultos mayores. En Chile un 70% de las heridas crónicas corresponden a UV y la prevalencia de UPP en pacientes hospitalizados es de 28%. El objetivo de esta revisión es analizar la evidencia disponible respecto al tratamiento nutricional de individuos con UPP y UV. Estas úlceras tienen diferentes etiologías, pero ambas provocan un aumento de requerimientos energéticos, proteicos y de micronutrientes. La cicatrización de heridas depende de varios factores como: el tipo de úlcera, estado nutricional, patologías presentes, el tipo de curación y el tratamiento médico. La terapia nutricional establece en la mantención o aumento de peso de estos pacientes, administración adecuada de proteínas y suplementación de energía, proteínas o micronutrientes cuando se presente déficit. Palabras clave: Nutrición; Suplementos nutricionales; Úlcera por presión; Úlcera venosa.
Most of the biological impacts of Vitamin E, including the redox effects, have been raised from studies with α-tocopherol only, despite the fact that tocopherol-containing foods carry mixed tocopherol isomers. Here, we investigated the cellular mechanisms involved in the immediate antioxidant responses evoked by α-, γand δ-tocopherol in Caco-2 cells. In order to track the cytosolic redox impact, we performed imaging on cells expressing HyPer, a fluorescent redox biosensor, while cytosolic calcium fluctuations were monitored by means of Fura-2 dye and imaging. With this approach, we could observe fast cellular responses evoked by the addition of α-, γand δ-tocopherol at concentrations as low as 2.5 µM. Each isomer induced rapid and consistent increases in cytosolic calcium with fast kinetics, which were affected by chelation of extracellular Ca 2+ , suggesting that tocopherols promoted a calcium entry upon the contact with the plasma membrane. In terms of redox effects, δ-tocopherol was the only isomer that evoked a significant change in the HyPer signal at 5 µM. By mimicking Ca 2+ entry with ionomycin and monensin, a decline in the HyPer signal was induced as well. Finally, by silencing calcium with 1,2-bis(o-aminophenoxy)ethane-N,N,N ,N -tetraacetic acid (BAPTA), an intracellular Ca 2+ chelator, none of the isomers were able to induce redox changes. Altogether, our data indicate that an elevation in cytoplasmic Ca 2+ is necessary for the development of a tocopherol-induced antioxidant impact on the cytoplasm of Caco-2 cells reported by HyPer biosensor.
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