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For example, vitamins C and E deficiencies are known to cause DNA oxidation and chromosomal damage [ 26, 27].
Nutritional disturbances in patients with IBD include macro- and micronutrient deficiencies such as hypoproteinemia and hypoalbuminemia, electrolyte (calcium, magnesium, and potassium) and trace element (zinc, copper, and selenium) disturbances, vitamin (B12, A, complex B, C, D, and E) deficiencies, anemia (due to iron, B12, and folic acid deficiency), and loss of weight [ 9, 10].
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In experimental animals, the characteristic signs of induced vitamin E deficiency vary with the species.
Vitamin E deficiency is rare in humans, although it may develop in premature infants and in people with impaired fat absorption or metabolism.
Also, vitamin E deficiency was common (18%).
Vitamin E deficiency could cause hepatic necrosis in fish (Idris and Hassan, 2002).
Elevated dietary vitamin C reduced the incidence and severity of vitamin E deficiency signs in a dose-dependent manner.
We hypothesized that vitamin E (vit E) deficiency, which will increase oxidative stress, would augment the training-induced adaptation of antioxidant enzymes.
Undernutrition, obesity and vitamin E deficiency, as well as several metabolic risk factors for cardiovascular disease coexisted in this studied group.
A new research showed that oxidative stress induced by SWNT in C57BL/6 mice and Vitamin E deficiency enhances pulmonary inflammatory response [22].
Growth, survival, signs of vitamin E deficiency, and immune and stress responses were monitored in groups of 30 golden shiners (mean average initial weight=0.79 g) fed the diets to apparent satiation twice daily in triplicate aquaria for 14 19 weeks.
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