Bioavailability of vitamin C from mashed potatoes and potato chips after oral administration in healthy Japanese men.
ABSTRACT Potato (Solanum tuberosum) tubers contain vitamin C (VC) and commercial potato chips have more VC content per wet weight by dehydration during frying. However, intestinal absorption of VC from orally ingested potatoes and its transfer to the blood remains questionable. The present study was designed to determine whether the dietary consumption of potatoes affects VC concentration in plasma and urinary excretion of VC in human subjects. After overnight fasting, five healthy Japanese men between 22 and 27 years of age consumed 87 g mashed potatoes and 282 g potato chips. Each portion contained 50 mg of VC, 50 mg VC in mineral water and mineral water. Before and after a single episode of ingestion, blood and urine samples were collected every 30 min or 1 h for 8 h. When measured by subtraction of the initial baseline value before administration of potatoes from the values measured throughout the 8 h test period, plasma VC concentrations increased almost linearly up to 3 h. Subsequently, the values of potato-fed subjects were higher than those of water, but did not differ significantly from those of VC in water (P = 0·14 and P = 0·5). Less VC tended to be excreted in urine during the 8 h test than VC in water alone (17·0 (sem 7·5) and 25·9 (sem 8·8) v. 47·9 (sem 17·9) μmol/mmol creatinine). Upon human consumption, mashed potatoes and potato chips provide VC content that is effectively absorbed in the intestine and transferred to the blood. Clearly, potatoes are a readily available source of dietary VC.
- SourceAvailable from: Emile Van Schaftingen[show abstract] [hide abstract]
ABSTRACT: Vitamin C, a reducing agent and antioxidant, is a cofactor in reactions catalyzed by Cu(+)-dependent monooxygenases and Fe(2+)-dependent dioxygenases. It is synthesized, in vertebrates having this capacity, from d-glucuronate. The latter is formed through direct hydrolysis of uridine diphosphate (UDP)-glucuronate by enzyme(s) bound to the endoplasmic reticulum membrane, sharing many properties with, and most likely identical to, UDP-glucuronosyltransferases. Non-glucuronidable xenobiotics (aminopyrine, metyrapone, chloretone and others) stimulate the enzymatic hydrolysis of UDP-glucuronate, accounting for their effect to increase vitamin C formation in vivo. Glucuronate is converted to l-gulonate by aldehyde reductase, an enzyme of the aldo-keto reductase superfamily. l-Gulonate is converted to l-gulonolactone by a lactonase identified as SMP30 or regucalcin, whose absence in mice leads to vitamin C deficiency. The last step in the pathway of vitamin C synthesis is the oxidation of l-gulonolactone to l-ascorbic acid by l-gulonolactone oxidase, an enzyme associated with the endoplasmic reticulum membrane and deficient in man, guinea pig and other species due to mutations in its gene. Another fate of glucuronate is its conversion to d-xylulose in a five-step pathway, the pentose pathway, involving identified oxidoreductases and an unknown decarboxylase. Semidehydroascorbate, a major oxidation product of vitamin C, is reconverted to ascorbate in the cytosol by cytochrome b(5) reductase and thioredoxin reductase in reactions involving NADH and NADPH, respectively. Transmembrane electron transfer systems using ascorbate or NADH as electron donors serve to reduce semidehydroascorbate present in neuroendocrine secretory vesicles and in the extracellular medium. Dehydroascorbate, the fully oxidized form of vitamin C, is reduced spontaneously by glutathione, as well as enzymatically in reactions using glutathione or NADPH. The degradation of vitamin C in mammals is initiated by the hydrolysis of dehydroascorbate to 2,3-diketo-l-gulonate, which is spontaneously degraded to oxalate, CO(2) and l-erythrulose. This is at variance with bacteria such as Escherichia coli, which have enzymatic degradation pathways for ascorbate and probably also dehydroascorbate.FEBS Journal 02/2007; 274(1):1-22. · 4.25 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: This research evaluates the ascorbic acid loss of vegetables prepared in a hospital cook-chill plated system. The ascorbic acid loss of three vegetable samples (carrots, peas and potatoes) were measured at various points in the cook-chill system and analysed using the DCPIP method. Substantial losses for all vegetables were identified at the cooking and regeneration stages. The ascorbic acid levels of the selected vegetables when raw ranged from 6 to 10 mg/100 g sample. At the end of the food service cycle the ascorbic acid content of the vegetables was reduced to 1.7-5.8 mg/100 g sample. The largest percentage loss of ascorbic acid, i.e. 76%, was found in mashed potatoes. Peas incurred the least percentage loss, i.e. 42%. This progressive deterioration during the cook-chill plated catering system causes an insubstantial presence of ascorbic acid in the food served to hospitalised patients.International Journal of Food Sciences and Nutrition 06/2001; 52(3):205-11. · 1.26 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: There are large inter-individual differences in the metabolism of vitamin C (VC), which is composed of both ascorbic acid (AsA) and dehydroascorbic acid (DAsA). AsA is oxidized to DAsA in a series of xenobiotic reactions. Thus, the effects of polymorphism A313G (Ile105Val) in the gene for glutathione S-transferases P1 (GSTP1), one of the most active xenobiotic enzymes, on human VC metabolism were studied. The variant frequency of GSTP1 among the present subjects (n=210) was AA 71.0%; GA 27.0% and GG 1.9%. At 24 h after administration of 1 mmol of VC to young women (n=17; age, 21.0+/-1.1 y), total VC excretion (46.7+/-18.1mg) by AA homozygotes of GSTP1 was greater (p<0.0069) than that (28.2+/-14.0 mg) by GA heterozygotes. One hour after administration of VC, blood total VC levels were also significantly different (p<0.0036) between the homozygotes and heterozygotes. The effects of other polymorphisms in xenobiotic enzymes on VC metabolism were small.Biochemical and Biophysical Research Communications 01/2008; 364(3):708-13. · 2.41 Impact Factor