Effect of vitamin E deficiency and supercritical fluid aerosolized vitamin E supplementation on interleukin-1-induced oxidative lung injury in rats

It is now established that vitamin E is an essential nutrient for all animals including man. It is now established that a deficiency of this vitamin, particularly in the infant, will result in a shortening of red cell life-span. The magnitude of the anemia appears related to the presence of associated factors such as the lipid composition of the red cell membrane and the nature of associated oxidant stresses. Healthy term infants who are fed either human milk or proprietary formulas in quantities sufficient to meet their caloric requirements will receive adequate amounts of vitamin E. The same appears to be true for small preterm infants even when the formulas are fortified with iron. Infants who are receiving inadequate volumes of formula should receive vitamin E supplementation of approximately 15 mg/day.

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Can Vitamin E Deficiency Occur in an Infant Receiving Total Parenteral Nutrition?

PEDIATRICS ◽

10.1542/peds.59.5.789 ◽

1977 ◽

Vol 59 (5) ◽

pp. 789-790

Author(s):

A. Myron Johnson ◽

Mary Ann Williams Morris

Keyword(s):

Vitamin E ◽

Parenteral Nutrition ◽

Total Parenteral Nutrition ◽

Premature Infants ◽

Newborn Infants ◽

Vitamin E Deficiency ◽

Gastrointestinal Obstruction ◽

Lipid Supplementation ◽

Upper Gastrointestinal ◽

Vitamin E Supplementation

Reports in the July 1975 issue of Pediatrics of total parenteral nutrition (TPN) in newborn infants, with and without lipid supplementation,1,2 have prompted a brief report of our experience with a small premature infant given TPN because of upper gastrointestinal obstruction and postoperative intolerance of enteral nutrition. Although cause-and-effect relationships are far from clear, this infant's course raises a question about the adequacy of vitamin E supplementation for premature infants receiving TPN. Case Report. F.I. (No. 31-10-62) was the first born in a pair of dizygotic black twins, weighed 1,370 gm, and was the product of a 30-week gestation terminated by spontaneous rupture of membranes.

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Vitamin E deficiency and metabolic deficits in neuronal ceroid lipofuscinosis described by bioinformatics

Physiological Genomics ◽

10.1152/physiolgenomics.00100.2002 ◽

2002 ◽

Vol 11 (3) ◽

pp. 195-203 ◽

Cited By ~ 31

Author(s):

J. L. Griffin ◽

D. Muller ◽

R. Woograsingh ◽

V. Jowatt ◽

A. Hindmarsh ◽

...

Keyword(s):

Vitamin E ◽

Neuronal Ceroid Lipofuscinosis ◽

Principal Component ◽

Dietary Supplementation ◽

Metabolic Phenotype ◽

Metabolic Abnormalities ◽

Cerebral Tissue ◽

Vitamin E Deficiency ◽

H Nmr ◽

Vitamin E Supplementation

The mnd mouse, a model of neuronal ceroid lipofusinosis (NCL), has a profound vitamin E deficiency in sera and brain, associated with cerebral deterioration characteristic of NCL. In this study, the vitamin E deficiency is corrected using dietary supplementation. However, the histopathological features associated with NCL remained. With use of a bioinformatics approach based on high-resolution solid and solution state 1H-NMR spectroscopy and principal component analysis (PCA), the deficits associated with NCL are defined in terms of a metabolic phenotype. Although vitamin E supplementation reversed some of the metabolic abnormalities, in particular the concentration of phenylalanine in extracts of cerebral tissue, PCA demonstrated that metabolic deficits associated with NCL were greater than any effects produced from vitamin E supplementation. These deficits included increased glutamate and N-acetyl-l-aspartate and decreased creatine and glutamine concentrations in aqueous extracts of the cortex, as well as profound accumulation of lipid in intact cerebral tissue. This is discussed in terms of faulty production of mitochondrial-associated membranes, thought to be central to the deficits in mnd mice.

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