[Lactose-induced diarrhea increases oxidative stress and it is more severe in rats deficient in vitamin E]. / La diarrea inducida con lactosa estimula la condición oxidativa y es más severa en ratas deficientes en vitamina E.

Diarrhea is the disease with high incidence in the world and causes infant mortality and malnutrition in the developing world. This justifies the study of nutrition and diarrhea. Due to ethical and financial considerations it is difficult to study nutrition and diarrhea in children thus animal models have become a convenient alternative. In previous studies it was shown that lactose induced diarrhea in rats was associated with a reduction in tissue levels of vitamin E and also with evidence of an inflammatory response of the intestine. Accordingly, in this study, in order to determine the effect of this type of diarrhea on the level of oxidative stress, diarrhea was induced in vitamin E sufficient and deficient rats. The results showed that after 23 days the tissue concentration of vitamin E decreased in all the rats with diarrhea but this reduction was substantially greater in the vitamin E deficient group. Moreover, diarrhea was 60% more severe in the vitamin E deficient rats than in the vitamin E sufficient group that also had diarrhea. Both diarrhea and vitamin E deficiency altered malonaldehyde and superoxide dismutase levels in various tissues. However, the most outstanding changes associated with diarrhea were a 100% increment in plasma malonaldehyde and erythrocyte superoxide dismutase activities which were 8 to 11 times higher than those seen in the rats without diarrhea. These non-invasive changes correlated well with the severity of diarrhea. The study shows that vitamin E deficiency results in diarrheas which are more severe and that lactose induced diarrhea is associated with higher levels of oxidative stress.

Funciones de la Vitamina E en la nutrición humana / Role of vitamin E in human nutrition

La vitamina E pertenece al grupo de vitaminas liposolubles ampliamente distribuida en los alimentos. Su principal función descrita es como antioxidante natural que reacciona con los radicales libres solubles en los lipidos de las membranas, también desempeña una función fisicoquímica en el ordenamiento de las membranas lipídicas, estabilizando las estructuras de membranas. Su absorción es relativamente pobre y va unida a los lípidos de la dieta. Se ha descrito neuropatía que comienza a partir del daño en la membrana axonal y decursa hacia una axonopatía distal que afecta las fibras mielinizadas de gran calibre. Las deficiencias de vitamina E son particularmente importante en los recién nacidos prematuros por sus deficientes reservas corporales y deterioro de la absorción de las grasas. La mayoría de las secuelas secundarias a la deficiencia de vitamina E son subclínicas, se han estudiado afectaciones en el sistema inmunológico relacionado con la deficiencia de la vitamina E en la proliferación celular y su función fagocítica. En las enfermedades crónicas no transmisibles y, particularmente, las cardiovasculares y el cáncer, se han estudiado las relaciones entre las vitaminas antioxidantes y sus fisiopatologías, no existiendo resultados consistentes y las fuerzas de asociación encontradas no son elevadas, ya que existen muchos factores de riesgo que son comunes a ambas enfermedades y modifican su aparición

Effect of vitamin E deficiency on neurologic function in patients with cystic fibrosis.

We evaluated neurologic function in 18 patients, ages 5 to 26 years, with cystic fibrosis. Eight were deficient in vitamin E. Sural nerve conduction latency was increased and nerve action potential amplitude decreased in the vitamin E-deficient group in comparison with the vitamin E-sufficient group. Two vitamin E-deficient patients had absent deep tendon reflexes; findings of clinical neurologic examinations were otherwise normal. We recommend early supplementation with vitamin E for patients with cystic fibrosis who have pancreatic insufficiency, to prevent neurologic dysfunction.