Ascorbic acid depletion enhances expression of the sodium-dependent vitamin C transporters, SVCT1 and SVCT2, and uptake of ascorbic acid in livers of SMP30/GNL knockout mice

Amano, Akiko; Aigaki, Toshiro; Maruyama, Naoki; Ishigami, Akihito

doi:10.1016/j.abb.2010.01.012

Cited by 52 publications

(35 citation statements)

References 34 publications

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“…16) Other studies have also indicated that AsA supplementation or deprivation influences AsA transport. 7,10,12) Our results also suggest that the peri-/ intracellular AsA level is an important regulator of SVCT1 and SVCT2 expression in the hepatocytes of ODS rats. Because the SVCT1 transporter is predominantly expressed in epithelial cells of the liver, an increase in hepatic SVCT1 levels can contribute to intracellular AsA accumulation in the liver.…”

Section: Abstract: 2-o--d-glucopyranosyl-l-ascorbicsupporting

confidence: 61%

“…11) Another study reported that AsA depletion enhanced the expression of SVCT1 and SVCT2 and the uptake of AsA in the livers of SMP30/GNL knockout mice. 12) SVCT2 mRNA levels were increased by the presence of fetal bovine serum and epidermal growth factor in human trophoblast cell line, 13) and by glucocorticoids, 14) zinc, 15) and calcium or phosphate ions in osteoblasts. 16) SVCT2 expression is downregulated during the differentiation of rat and mouse muscle cells.…”

Section: Abstract: 2-o--d-glucopyranosyl-l-ascorbicmentioning

confidence: 99%

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The Level of Orally Ingested Vitamin C Affected the Expression of Vitamin C Transporters and Vitamin C Accumulation in the Livers of ODS Rats

Sone

Ueta

Kodama

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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Section: Abstract: 2-o--d-glucopyranosyl-l-ascorbicsupporting

confidence: 61%

Section: Abstract: 2-o--d-glucopyranosyl-l-ascorbicmentioning

confidence: 99%

The Level of Orally Ingested Vitamin C Affected the Expression of Vitamin C Transporters and Vitamin C Accumulation in the Livers of ODS Rats

Sone

Ueta

Kodama

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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“…In the latter study, the decrease in AA uptake upon supplementation was associated with a decrease in the level of expression of hSVCT-1. In contrast, an induction in the level of expression of SVCT-1 in the intestine of SMP30/GNI-knockout mice (animals that have lost the ability to synthesize AA endogenously) was observed upon feeding a vitamin C-deficient diet [22]. …”

Section: Ascorbatementioning

confidence: 99%

Intestinal absorption of water-soluble vitamins in health and disease

Said

2011

Biochemical Journal

335

239

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Our knowledge of the mechanisms and regulation of intestinal absorption of water-soluble vitamins under normal physiological conditions, and of the factors/conditions that affect and interfere with theses processes has been significantly expanded in recent years as a result of the availability of a host of valuable molecular/cellular tools. Although structurally and functionally unrelated, the water-soluble vitamins share the feature of being essential for normal cellular functions, growth and development, and that their deficiency leads to a variety of clinical abnormalities that range from anaemia to growth retardation and neurological disorders. Humans cannot synthesize water-soluble vitamins (with the exception of some endogenous synthesis of niacin) and must obtain these micronutrients from exogenous sources. Thus body homoeostasis of these micronutrients depends on their normal absorption in the intestine. Interference with absorption, which occurs in a variety of conditions (e.g. congenital defects in the digestive or absorptive system, intestinal disease/resection, drug interaction and chronic alcohol use), leads to the development of deficiency (and sub-optimal status) and results in clinical abnormalities. It is well established now that intestinal absorption of the water-soluble vitamins ascorbate, biotin, folate, niacin, pantothenic acid, pyridoxine, riboflavin and thiamin is via specific carrier-mediated processes. These processes are regulated by a variety of factors and conditions, and the regulation involves transcriptional and/or post-transcriptional mechanisms. Also well recognized now is the fact that the large intestine possesses specific and efficient uptake systems to absorb a number of water-soluble vitamins that are synthesized by the normal microflora. This source may contribute to total body vitamin nutrition, and especially towards the cellular nutrition and health of the local colonocytes. The present review aims to outline our current understanding of the mechanisms involved in intestinal absorption of water-soluble vitamins, their regulation, the cell biology of the carriers involved and the factors that negatively affect these absorptive events.

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“…Therefore, SMP30/GNL knockout (KO) mice lack any ability to synthesize AA in vivo (21,22 rate of pulmonary emphysema (23), susceptibility to ultraviolet radiation (UVR)-induced cataracts (24), epidermal atrophy, and extensive ultraviolet B (UVB)-induced skin pigmentation (25) as well as a decrease in skin collagen content, and hair growth (26). Moreover, the expression of sodium-dependent vitamin C transporter (SVCT) 1 and 2 in the liver increased (27). Using this SMP30/GNL KO murine model, we also reported that an AA deficiency increased superoxide formation in the brain (28,29), but those values in other tissues are still unknown.…”

mentioning

confidence: 99%

Effects of Ascorbic Acid Deficiency on Protein and Lipid Oxidation in Livers from SMP30/GNL Knockout Mice

Amano

Sato

Kishimoto

et al. 2013

J Nutr Sci Vitaminol

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Summary Ascorbic acid (AA) functions as an electron donor and scavenges reactive oxygen species such as superoxide, singlet oxygen, and hydroxyl radicals in vitro. However, little is known about the effect of an AA deficiency on protein and lipid oxidation levels in the liver. Therefore, we measured the levels of protein carbonyl and thiobarbituric acid reactive substances (TBARS) in livers from senescence marker protein-30 (SMP30)/gluconolactonase (GNL) knockout (KO) mice. These mice are deficient in AA, because they lack the SMP30/GNL gene, which is essential for the biosynthesis of AA in vivo. To track the effect of an AA deficiency, at 30 d of age, mice were divided into the following four groups: AA (2) SMP30/GNL KO, AA (1) SMP30/GNL KO, AA (2) wild type (WT), and AA (1) WT. The AA (1) groups were given water containing 1.5 g/L AA, whereas the AA (2) groups received water without AA for 57 d. All mice were fed an AA-free diet. Subsequently, protein carbonyl levels in livers from AA (2) SMP30/GNL KO mice were significantly higher than those from the other three groups; however, TBARS levels were not significantly different among the four groups. Therefore, AA must act as an anti-oxidant for proteins but might not directly protect lipid oxidation in the liver.

show abstract

Ascorbic acid depletion enhances expression of the sodium-dependent vitamin C transporters, SVCT1 and SVCT2, and uptake of ascorbic acid in livers of SMP30/GNL knockout mice

Cited by 52 publications

References 34 publications

The Level of Orally Ingested Vitamin C Affected the Expression of Vitamin C Transporters and Vitamin C Accumulation in the Livers of ODS Rats

The Level of Orally Ingested Vitamin C Affected the Expression of Vitamin C Transporters and Vitamin C Accumulation in the Livers of ODS Rats

Intestinal absorption of water-soluble vitamins in health and disease

Effects of Ascorbic Acid Deficiency on Protein and Lipid Oxidation in Livers from SMP30/GNL Knockout Mice

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