Effect of vitamin E on memranes of the intestinal cell.

Molenaar, I.; Hommes, F. A.; Braams, W G; Polman, H. A.

doi:10.1073/pnas.61.3.982

Cited by 36 publications

(5 citation statements)

References 6 publications

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“…Throughout this study, no subject developed any complication of chronic liver disease, such as worsening previous demonstration by Molenaar et al (22,23) of ultrastructural changes in intestinal epithelial cellular membranes in vitamin E-deficient ducklings and man, we postulated that intestinal absorptive function would be impaired in the human vitamin E deficiency state. However, in the present study, we detected no change in intestinal malabsorption of either fat or vitamin E following the correction of vitamin E deficiency, suggesting that the impaired absorption of both of these nutrients in our patients was not due to an effect of vitamin E on intestinal mucosal function.…”

Section: -supporting

confidence: 57%

Correction of vitamin E deficiency in children with chronic cholestasis. II. Effect on gastrointestinal and hepatic function

et al. 1986

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Although secondary vitamin E deficiency causes a reversible neurologic disorder in children with chronic cholestasis, the effect of this deficiency state on other organ systems is unknown. We studied the effects of vitamin E therapy on selected gastrointestinal and hepatic functions in five children with chronic cholestasis and well-documented biochemical and neurologic evidence of vitamin E deficiency. After 2 to 3 years of oral or parenteral vitamin E therapy, there was no improvement in fecal fat losses, severity of vitamin E malabsorption (as measured by an oral vitamin E tolerance test) or total serum fatty acid concentrations. Serial analyses of liver function blood tests demonstrated a marked decline in fasting serum cholylglycine concentrations during 18 to 31 months of vitamin E therapy, while other liver function tests showed no consistent changes. We conclude that vitamin E deficiency does not appear to alter intestinal absorption of fat or vitamin E; however, vitamin E deficiency may further impair already compromised hepatic function during pathologic conditions such as cholestasis.

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Section: -supporting

confidence: 57%

Correction of vitamin E deficiency in children with chronic cholestasis. II. Effect on gastrointestinal and hepatic function

et al. 1986

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“…4) is of profound interest especially when referred to the previously reported electron microscopic findings of DJACZENKO et al (64) and CAYGILL (65) in the appearance of the liver mitochondria and endoplasmic reticulum of E-deficient rats, such as swelling, loss of electron density of matrix and a decrease in the number of cristae (in mitochondria), and morphological alteration with consequent fragmentation and eventual disappear of the fragments (in endoplasmic reticulum). Meanwhile, a histochemical study by electron microscopy suggested a possible role of vitamin E in maintaining normal structures of intracellular membranes by its capacity to increase unsaturated fatty acid incorporation into the membrane as well as inhibit decomposition of these unsaturated fatty acids (66). This hypo thesis is supported by our results that unsaturation of fatty acid of phospholipid in liver declines with vitamin E deficiency ( Table 2, Table 3).…”

Section: Vitaminsupporting

confidence: 70%

A Mechanism of the Acceleration of Lipid Peroxide Formation in Liver Homogenates and Subcellular Fractions of Vitamin E-Deficient Mice

Fukuzawa

Uchiyama

1973

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…Recent evidence suggests that c~-tocopherol may play an important role in membrane metabolism and structure [11]. Further experiments will be necessary to elucidate the exact role of e-tocopherol in the visual apparatus.…”

Section: P R O D U C T C O M P a R E D To P U R E ~-T O C O P H E R Ymentioning

confidence: 99%

Alpha-tocopherol in the retinal outer segment of bovine eyes

Dilley¹,

McConnell

1970

J. Membrain Biol.

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α-Tocopherol was identified in lipid extracts of bovine retinal outer segment (ROS) preparations. Positive identification was obtained by the thin layer chromatographic characteristics of the tocopherol form and its oxidation product α-tocopherylquinone, and by the ultraviolet spectrum of the oxidized and KBH4-reduced form of the tocopherylquinone. In the ROS preparations used, α-tocopherol chromanol was the predominant species, the quinone form accounting for 25% or less of the total. The concentration of α-tocopherol in the ROS preparations was about 0.1 mole α-tocopherol per mole rhodopsin, or about 1 nmole/mg, protein. Mitochondria from bovine retina contained about 0.4 nmole α-tocopherol per mg protein.

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Effect of vitamin E on memranes of the intestinal cell.

Cited by 36 publications

References 6 publications

Correction of vitamin E deficiency in children with chronic cholestasis. II. Effect on gastrointestinal and hepatic function

Correction of vitamin E deficiency in children with chronic cholestasis. II. Effect on gastrointestinal and hepatic function

A Mechanism of the Acceleration of Lipid Peroxide Formation in Liver Homogenates and Subcellular Fractions of Vitamin E-Deficient Mice

Alpha-tocopherol in the retinal outer segment of bovine eyes

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