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Mark Levine - One of the best experts on this subject based on the ideXlab platform.
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temporo spacial microanatomical distribution of the murine sodium dependent ascorbic acid transporters SLC23A1 and slc23a2 in the kidney throughout development
Biochemistry and Cell Biology, 2017Co-Authors: Peter Eck, Christopher Corpe, Mark LevineAbstract:The two membrane transporters SLC23A1 and Slc23a2 mediate ascorbic acid uptake into cells. We recently determined the key role of SLC23A1 in renal re-absorption of ascorbic acid in a knockout mouse...
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identification and functional characterization of an alternative 5 exon of the sodium dependent ascorbic acid transporter SLC23A1 818 5
The FASEB Journal, 2014Co-Authors: Mandana Amir Shaghaghi, Mark Levine, Natalia Yurkova, Peter EckAbstract:Vitamin C, an essential micronutrient and a critical cofactor for several intracellular enzymatic reactions, is actively transported across epithelial barriers through the sodium-dependent ascorbic acid transporter 1 (SLC23A1). The SLC23A1 gene encodes SLC23A1 transporter and is located on human chromosome 5q31.2 (138702885-138719039 compl.; NC_000005.9). Previously, the SLC23A1 transcript has been described as containing 15 exons, stretching over 16 kilobases; however, no alternative splice variant has been described yet. Variations in SLC23A1 gene would impact vitamin C dietary requirements and/or susceptibility to common complex diseases. We have, therefore, evaluated the existence of additional SLC23A1 transcripts in silico and examined the function of new transcript through Xenopus laevis oocytes injection. Here, we characterized a novel alternative first exon encoding a SLC23A1 isoform which is exclusive to human and is expressed in the small intestine. The novel SLC23A1 protein isoform adds 36 N-te...
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the human sodium dependent ascorbic acid transporters SLC23A1 and slc23a2 do not mediate ascorbic acid release in the proximal renal epithelial cell
Physiological Reports, 2013Co-Authors: Peter Eck, Oran Kwon, Shenglin Chen, Omar Y Mian, Mark LevineAbstract:Sodium-dependent ascorbic acid membrane transporters SLC23A1 and SLC23A2 mediate ascorbic acid (vitamin C) transport into cells. However, it is unknown how ascorbic acid undergoes cellular release, or efflux. We hypothesized that SLC23A1 and SLC23A2 could serve a dual role, mediating ascorbic acid cellular efflux as well as uptake. Renal reabsorption is required for maintaining systemic vitamin C concentrations. Because efflux from nephron cells is necessary for reabsorption, we studied whether SLC23A1 and SLC23A2 mediate efflux of ascorbic acid in the human renal nephron. We found high gene expression of SLC23A1 but no expression of SLC23A2 in the proximal convoluted and straight tubules of humans. These data rule out SLC23A2 as the ascorbic acid release protein in the renal proximal tubular epithelia cell. We utilized a novel dual transporter-based Xenopus laevis oocyte system to investigate the function of the SLC23A1 protein, and found that no ascorbate release was mediated by SLC23A1. These findings were confirmed in mammalian cells overexpressing SLC23A1. Taken together, the data for SLC23A1 show that it too does not have a role in cellular release of ascorbic acid across the basolateral membrane of the proximal tubular epithelial cell, and that SLC23A1 alone is responsible for ascorbic acid uptake across the apical membrane. These findings reiterate the physiological importance of proper functioning of SLC23A1 in maintaining vitamin C levels for health and disease prevention. The ascorbate efflux mechanism in the proximal tubule of the kidney remains to be characterized.
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genetic variation in sodium dependent vitamin c transporters SLC23A1 and slc23a2 and risk of advanced colorectal adenoma
Nutrition and Cancer, 2008Co-Authors: Hans Christian Erichsen, Mark Levine, Peter Eck, Robert Welch, Meredith Yeager, Ulrike Peters, Robert E Schoen, Richard B Hayes, Stephen J ChanockAbstract:Previous observational studies suggest that vitamin C may reduce risk of colorectal cancer. Vitamin C transport is facilitated by membrane bound sodium-dependent transporters, SVCT1 (encoded by SLC23A1) and SVCT2 (encoded by SLC23A2). To investigate if common genetic variants in these two genes are associated with risk of colorectal tumor development, we conducted a case-control study of 656 Caucasian advanced distal colorectal adenoma cases and 665 Caucasian sigmoidoscopy-negative controls nested within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. The analysis of common single nucleotide polymorphisms in SLC23A1 revealed no association. For SLC23A2, overall, there was no association with haplotypes, but two SNPs located in intron 8 and exon 11 could be associated (odds ratio = 0.49, 95% confidence interval = 0.25-0.95 for haplotype G-C vs. haplotype C-C). The findings should be confirmed in follow-up studies, and further investigation is required to probe the functional basis of this finding.
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genomic and functional analysis of the sodium dependent vitamin c transporter SLC23A1 svct1
Genes and Nutrition, 2007Co-Authors: Christopher Corpe, Peter Eck, Hans Christian Erichsen, Stephen J Chanock, James G. Taylor, Mark LevineAbstract:Vitamin C, an essential co-factor for at least eight enzymatic reactions, might also be involved in development or treatment of cancer, cardiovascular diseases, diabetes, and stroke. Ascorbic acid, the reduced form of vitamin C is transported across epithelial barriers by the sodium dependent vitamin C transporters 1 (SVCT1). SVCT1 is encoded by SLC23A1 and mapped to 5q31.2 [1, 2]. Recently, the pattern of common genetic variants has been characterized for both ascorbic acid transporters, SLC23A1 and SLC23A2, which share common intron/exon borders, are 58% similar in sequence across the coding region, but differ greatly in size and linkage disequilibrium patterns [3]. Here we characterize the genetic variation in the less constrained SLC23A1 gene in more detail and test for functional consequences. SLC23A1 is expressed in tissues critical for absorption and reabsorption of vitamin C (kidney, intestinal, and hepatic tissues) [4]. Therefore functional consequences of variations in SVCT1 would impact on dietary requirements and recommendations.
Peter Eck - One of the best experts on this subject based on the ideXlab platform.
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temporo spacial microanatomical distribution of the murine sodium dependent ascorbic acid transporters SLC23A1 and slc23a2 in the kidney throughout development
Biochemistry and Cell Biology, 2017Co-Authors: Peter Eck, Christopher Corpe, Mark LevineAbstract:The two membrane transporters SLC23A1 and Slc23a2 mediate ascorbic acid uptake into cells. We recently determined the key role of SLC23A1 in renal re-absorption of ascorbic acid in a knockout mouse...
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identification and functional characterization of an alternative 5 exon of the sodium dependent ascorbic acid transporter SLC23A1 818 5
The FASEB Journal, 2014Co-Authors: Mandana Amir Shaghaghi, Mark Levine, Natalia Yurkova, Peter EckAbstract:Vitamin C, an essential micronutrient and a critical cofactor for several intracellular enzymatic reactions, is actively transported across epithelial barriers through the sodium-dependent ascorbic acid transporter 1 (SLC23A1). The SLC23A1 gene encodes SLC23A1 transporter and is located on human chromosome 5q31.2 (138702885-138719039 compl.; NC_000005.9). Previously, the SLC23A1 transcript has been described as containing 15 exons, stretching over 16 kilobases; however, no alternative splice variant has been described yet. Variations in SLC23A1 gene would impact vitamin C dietary requirements and/or susceptibility to common complex diseases. We have, therefore, evaluated the existence of additional SLC23A1 transcripts in silico and examined the function of new transcript through Xenopus laevis oocytes injection. Here, we characterized a novel alternative first exon encoding a SLC23A1 isoform which is exclusive to human and is expressed in the small intestine. The novel SLC23A1 protein isoform adds 36 N-te...
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the human sodium dependent ascorbic acid transporters SLC23A1 and slc23a2 do not mediate ascorbic acid release in the proximal renal epithelial cell
Physiological Reports, 2013Co-Authors: Peter Eck, Oran Kwon, Shenglin Chen, Omar Y Mian, Mark LevineAbstract:Sodium-dependent ascorbic acid membrane transporters SLC23A1 and SLC23A2 mediate ascorbic acid (vitamin C) transport into cells. However, it is unknown how ascorbic acid undergoes cellular release, or efflux. We hypothesized that SLC23A1 and SLC23A2 could serve a dual role, mediating ascorbic acid cellular efflux as well as uptake. Renal reabsorption is required for maintaining systemic vitamin C concentrations. Because efflux from nephron cells is necessary for reabsorption, we studied whether SLC23A1 and SLC23A2 mediate efflux of ascorbic acid in the human renal nephron. We found high gene expression of SLC23A1 but no expression of SLC23A2 in the proximal convoluted and straight tubules of humans. These data rule out SLC23A2 as the ascorbic acid release protein in the renal proximal tubular epithelia cell. We utilized a novel dual transporter-based Xenopus laevis oocyte system to investigate the function of the SLC23A1 protein, and found that no ascorbate release was mediated by SLC23A1. These findings were confirmed in mammalian cells overexpressing SLC23A1. Taken together, the data for SLC23A1 show that it too does not have a role in cellular release of ascorbic acid across the basolateral membrane of the proximal tubular epithelial cell, and that SLC23A1 alone is responsible for ascorbic acid uptake across the apical membrane. These findings reiterate the physiological importance of proper functioning of SLC23A1 in maintaining vitamin C levels for health and disease prevention. The ascorbate efflux mechanism in the proximal tubule of the kidney remains to be characterized.
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vitamin c transporter SLC23A1 links renal reabsorption vitamin c tissue accumulation and perinatal survival in mice
Journal of Clinical Investigation, 2010Co-Authors: Christopher Corpe, Yaohui Wang, Peter Eck, Jin Wang, Robert Faulhaberwalter, Jurgen Schnermann, Sam Margolis, Sebastian J Padayatty, He Sun, Robert L NussbaumAbstract:Levels of the necessary nutrient vitamin C (ascorbate) are tightly regulated by intestinal absorption, tissue accumulation, and renal reabsorption and excretion. Ascorbate levels are controlled in part by regulation of transport through at least 2 sodium-dependent transporters: SLC23A1 and Slc23a2 (also known as Svct1 and Svct2, respectively). Previous work indicates that Slc23a2 is essential for viability in mice, but the roles of SLC23A1 for viability and in adult physiology have not been determined. To investigate the contributions of SLC23A1 to plasma and tissue ascorbate concentrations in vivo, we generated SLC23A1-/- mice. Compared with wild-type mice, SLC23A1-/- mice increased ascorbate fractional excretion up to 18-fold. Hepatic portal ascorbate accumulation was nearly abolished, whereas intestinal absorption was marginally affected. Both heterozygous and knockout pups born to SLC23A1-/- dams exhibited approximately 45% perinatal mortality, and this was associated with lower plasma ascorbate concentrations in dams and pups. Perinatal mortality of SLC23A1-/- pups born to SLC23A1-/- dams was prevented by ascorbate supplementation during pregnancy. Taken together, these data indicate that ascorbate provided by the dam influenced perinatal survival. Although SLC23A1-/- mice lost as much as 70% of their ascorbate body stores in urine daily, we observed an unanticipated compensatory increase in ascorbate synthesis. These findings indicate a key role for SLC23A1 in renal ascorbate absorption and perinatal survival and reveal regulation of vitamin C biosynthesis in mice.
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genetic variation in sodium dependent vitamin c transporters SLC23A1 and slc23a2 and risk of advanced colorectal adenoma
Nutrition and Cancer, 2008Co-Authors: Hans Christian Erichsen, Mark Levine, Peter Eck, Robert Welch, Meredith Yeager, Ulrike Peters, Robert E Schoen, Richard B Hayes, Stephen J ChanockAbstract:Previous observational studies suggest that vitamin C may reduce risk of colorectal cancer. Vitamin C transport is facilitated by membrane bound sodium-dependent transporters, SVCT1 (encoded by SLC23A1) and SVCT2 (encoded by SLC23A2). To investigate if common genetic variants in these two genes are associated with risk of colorectal tumor development, we conducted a case-control study of 656 Caucasian advanced distal colorectal adenoma cases and 665 Caucasian sigmoidoscopy-negative controls nested within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. The analysis of common single nucleotide polymorphisms in SLC23A1 revealed no association. For SLC23A2, overall, there was no association with haplotypes, but two SNPs located in intron 8 and exon 11 could be associated (odds ratio = 0.49, 95% confidence interval = 0.25-0.95 for haplotype G-C vs. haplotype C-C). The findings should be confirmed in follow-up studies, and further investigation is required to probe the functional basis of this finding.
James R. Hammond - One of the best experts on this subject based on the ideXlab platform.
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changes in aortic reactivity associated with the loss of equilibrative nucleoside transporter 1 ent1 in mice
PLOS ONE, 2018Co-Authors: Arielle K. Best, James R. Hammond, Derek B. Bone, Robert Gros, Gonzalo L VilasAbstract:Slc29a1 encodes for equilibrative nucleoside transporter subtype 1 (ENT1), the primary mechanism of adenosine transfer across cell membranes. Previous studies showed that tissues isolated from Slc29a1-null mice are relatively resistant to injury caused by vascular ischemia-reperfusion. To determine if there are similar changes in the microvasculature, and investigate underlying mechanism, we examined aortas isolated from wildtype and Slc29a1-null mice. Aorta macrostructure and gene expression were examined histologically and by qPCR, respectively. Wire myography was used to assess the contractile properties of isolated thoracic aortic rings and their response to adenosine under both normoxic and hypoxic conditions. In vivo haemodynamic parameters were assessed using the tail-cuff method. Slc29a1-null mice had significantly (P<0.05) increased plasma adenosine (2.75-fold) and lower blood pressure (~15% ↓) than wild-type mice. Aortas from Slc29a1-null mice were stiffer with a smaller circumference (11% ↓), and had an enhanced contractile response to KCl and receptor-mediated stimuli. Blockade of ENT1 with nitrobenzylthioinosine significantly enhanced (by ~3.5-fold) the response of aorta from wild-type mice to phenylephrine, but had minimal effect on aortas from Slc29a1-null mice. Adenosine enhanced phenylephrine-mediated constriction in the wild-type tissue under both normoxic (11.7-fold) and hypoxic (3.6-fold) conditions, but had no effect on the Slc29a1-null aortic aorta. In conclusion, aortas from Slc29a1-null mice respond to hypoxic insult in a manner comparable to wild-type tissues that have been pharmacologically preconditioned with adenosine. These data also support a role for ENT1 in the regulation of the protective effects of adenosine on contractile function in elastic conduit arteries such as thoracic aorta.
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Changes in aortic reactivity associated with the loss of equilibrative nucleoside transporter 1 (ENT1) in mice
2018Co-Authors: Arielle K. Best, Derek B. Bone, Gonzalo Vilas, Robert Gros, James R. HammondAbstract:Slc29a1 encodes for equilibrative nucleoside transporter subtype 1 (ENT1), the primary mechanism of adenosine transfer across cell membranes. Previous studies showed that tissues isolated from Slc29a1-null mice are relatively resistant to injury caused by vascular ischemia-reperfusion. To determine if there are similar changes in the microvasculature, and investigate underlying mechanism, we examined aortas isolated from wildtype and Slc29a1-null mice. Aorta macrostructure and gene expression were examined histologically and by qPCR, respectively. Wire myography was used to assess the contractile properties of isolated thoracic aortic rings and their response to adenosine under both normoxic and hypoxic conditions. In vivo haemodynamic parameters were assessed using the tail-cuff method. Slc29a1-null mice had significantly (P
Rahmatul Firdaushty - One of the best experts on this subject based on the ideXlab platform.
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gambaran polimorfisme gen slc22a1 rs683369 pada pasien diabetes melitus tipe 2 yang mendapatkan terapi metformin
Jurnal Kesehatan Andalas, 2020Co-Authors: Rahmatul Firdaushty, Elly Usman, Linosefa LinosefaAbstract:Mekanisme kerja metformin dipengaruhi oleh Organic Cation Transporter 1 (OCT1) yang dikode oleh gen SLC22A1. Variasi atau polimorfisme pada gen SLC22A1 mempengaruhi uptake metformin ke hati sehingga berhubungan dengan efek metformin dalam menurunkan glukosa darah. Rs683369 merupakan salah satu polimorfisme dari gen SLC22A1. Tujuan: Melihat gambaran polimorfisme gen SLC22A1 rs683369 pada pasien diabetes melitus tipe 2 yang mendapatkan terapi metfomin. Metode: Penelitian ini merupakan studi deskriptif dengan teknik consequtive sampling. Sampel berasal dari 44 pasien DM tipe 2 yang mendapatkan terapi tunggal metformin yang diambil darahnya melalui pembuluh vena untuk dilakukan pemeriksaan genotip dengan cara isolasi DNA, PCR dan sekuensing. Hasil: Didapatkan pasien DM tipe 2 yang mendapatkan terapi tunggal metformin sebagian besar adalah perempuan 63,6%, dan rerata umur 55,77±7,77 tahun. Pemerikaan genotip didapatkan hasil wild type (GG) 4,5%, mutan heterozigot (GC) 22,%, dan mutan homozigot (CC) 72,7%. Simpulan: Ditemukan polimorfisme gen SLC22A1 rs683369 pada pasien DM tipe 2 yang mendapatkan terapi metformin. Perlu penelitian lebih lanjut mengenai variasi lain pada gen SLC22A1 dan efeknya terhadap gula darah pasien.
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Gambaran Polimorfisme Gen SLC22A1 rs683369 pada Pasien Diabetes Melitus Tipe 2 yang Mendapatkan Terapi Metformin
2019Co-Authors: Rahmatul FirdaushtyAbstract:Metformin merupakan terapi lini pertama dalam pengobatan diabetes melitus (DM) tipe 2 di Indonesia. Mekanisme kerja metformin dipengaruhi oleh Organic Cation Transporter 1 (OCT1) yang dikode oleh gen SLC22A1.Variasi atau polimorfisme pada gen SLC22A1 mempengaruhi uptake metformin ke hati sehingga berhubungan dengan efek metformin dalam menurunkan glukosa darah. Rs683369 merupakan salah satu polimorfisme dari gen SLC22A1. Tujuan penelitian ini adalah untuk melihat gambaran polimorfisme gen SLC22A1 rs683369 pada pasien diabetes melitus tipe 2 yang mendapatkan terapi metfomin. Penelitian ini merupakan penelitian deskriptif dengan teknik consequtive sampling. Sampel berasal dari 44 pasien DM tipe 2 yang mendapatkan terapi tunggal metformin yang diambil darahnya melalui pembuluh vena untuk dilakukan pemeriksaan genotip dengan cara isolasi DNA, PCR dan sekuensing. Hasil penelitian ini ditemukan pasien DM tipe 2 yang mendapatkan terapi tunggal metformin sebagian besar adalah perempuan 63,6%, dan rerata umur 55,77±7,77 tahun. Pemerikaan genotip didapatkan hasil wildtype (GG) 4,5%, mutan heterozigot (GC) 22,%, dan mutan homozigot (CC) 72,7%. Kesimpulan penelitian ini adalah ditemukan adanya polimorfisme gen SLC22A1 rs683369 pada pasien DM tipe 2 yang mendapatkan terapi metformin. Perlu penelitian lebih lanjut mengenai variasi lain pada gen SLC22A1 dan efeknya terhadap gula darah pasien
Astrid E. Fletcher - One of the best experts on this subject based on the ideXlab platform.
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polymorphisms in sodium dependent vitamin c transporter genes and plasma aqueous humor and lens nucleus ascorbate concentrations in an ascorbate depleted setting
Experimental Eye Research, 2014Co-Authors: Srinivasan Senthilkumari, Badri Talwar, Kuppamuthu Dharmalingam, Ravilla D Ravindran, Ramamurthy Jayanthi, Charu Saravanan, Ian S Young, Periasamy Sundaresan, Alan D Dangour, Astrid E. FletcherAbstract:Abstract We have previously reported low concentrations of plasma ascorbate and low dietary vitamin C intake in the older Indian population and a strong inverse association of these with cataract. Little is known about ascorbate levels in aqueous humor and lens in populations habitually depleted of ascorbate and no studies in any setting have investigated whether genetic polymorphisms influence ascorbate levels in ocular tissues. Our objectives were to investigate relationships between ascorbate concentrations in plasma, aqueous humor and lens and whether these relationships are influenced by Single Nucleotide Polymorphisms (SNPs) in sodium-dependent vitamin C transporter genes (SLC23A1 and SLC23A2). We enrolled sixty patients (equal numbers of men and women, mean age 63 years) undergoing small incision cataract surgery in southern India. We measured ascorbate concentrations in plasma, aqueous humor and lens nucleus using high performance liquid chromatography. SLC23A1 SNPs (rs4257763, rs6596473) and SLC23A2 SNPs (rs1279683 and rs12479919) were genotyped using a TaqMan assay. Patients were interviewed for lifestyle factors which might influence ascorbate. Plasma vitamin C was normalized by a log 10 transformation. Statistical analysis used linear regression with the slope of the within-subject associations estimated using beta ( β ) coefficients. The ascorbate concentrations (μmol/L) were: plasma ascorbate, median and inter-quartile range (IQR), 15.2 (7.8, 34.5), mean (SD) of aqueous humor ascorbate, 1074 (545) and lens nucleus ascorbate, 0.42 (0.16) (μmol/g lens nucleus wet weight). Minimum allele frequencies were: rs1279683 (0.28), rs12479919 (0.30), rs659647 (0.48). Decreasing concentrations of ocular ascorbate from the common to the rare genotype were observed for rs6596473 and rs12479919. The per allele difference in aqueous humor ascorbate for rs6596473 was −217 μmol/L, p p β coefficients for the regression of log 10 plasma ascorbate on aqueous humor ascorbate were higher for the GG genotype of rs6596473: GG, β = 1460 compared to carriage of the C allele, CG, β = 1059, CC, β = 1132, p interaction = 0.1. In conclusion we found that compared to studies in well-nourished populations, ascorbate concentrations in the plasma, aqueous humor and lens nucleus were low. We present novel findings that polymorphisms in SLC23A1/2 genes influenced ascorbate concentration in aqueous humor and lens nucleus.
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polymorphisms in sodium dependent vitamin c transporter genes and plasma aqueous humor and lens nucleus ascorbate concentrations in an ascorbate depleted setting
Experimental Eye Research, 2014Co-Authors: Srinivasan Senthilkumari, Badri Talwar, Kuppamuthu Dharmalingam, Ravilla D Ravindran, Ramamurthy Jayanthi, Charu Saravanan, Ian S Young, Periasamy Sundaresan, Alan D Dangour, Astrid E. FletcherAbstract:We have previously reported low concentrations of plasma ascorbate and low dietary vitamin C intake in the older Indian population and a strong inverse association of these with cataract. Little is known about ascorbate levels in aqueous humor and lens in populations habitually depleted of ascorbate and no studies in any setting have investigated whether genetic polymorphisms influence ascorbate levels in ocular tissues. Our objectives were to investigate relationships between ascorbate concentrations in plasma, aqueous humor and lens and whether these relationships are influenced by Single Nucleotide Polymorphisms (SNPs) in sodium-dependent vitamin C transporter genes (SLC23A1 and SLC23A2). We enrolled sixty patients (equal numbers of men and women, mean age 63 years) undergoing small incision cataract surgery in southern India. We measured ascorbate concentrations in plasma, aqueous humor and lens nucleus using high performance liquid chromatography. SLC23A1 SNPs (rs4257763, rs6596473) and SLC23A2 SNPs (rs1279683 and rs12479919) were genotyped using a TaqMan assay. Patients were interviewed for lifestyle factors which might influence ascorbate. Plasma vitamin C was normalized by a log10 transformation. Statistical analysis used linear regression with the slope of the within-subject associations estimated using beta (β) coefficients. The ascorbate concentrations (μmol/L) were: plasma ascorbate, median and inter-quartile range (IQR), 15.2 (7.8, 34.5), mean (SD) of aqueous humor ascorbate, 1074 (545) and lens nucleus ascorbate, 0.42 (0.16) (μmol/g lens nucleus wet weight). Minimum allele frequencies were: rs1279683 (0.28), rs12479919 (0.30), rs659647 (0.48). Decreasing concentrations of ocular ascorbate from the common to the rare genotype were observed for rs6596473 and rs12479919. The per allele difference in aqueous humor ascorbate for rs6596473 was -217 μmol/L, p < 0.04 and a per allele difference in lens nucleus ascorbate of -0.085 μmol/g, p < 0.02 for rs12479919. The β coefficients for the regression of log10 plasma ascorbate on aqueous humor ascorbate were higher for the GG genotype of rs6596473: GG, β = 1460 compared to carriage of the C allele, CG, β = 1059, CC, β = 1132, p interaction = 0.1. In conclusion we found that compared to studies in well-nourished populations, ascorbate concentrations in the plasma, aqueous humor and lens nucleus were low. We present novel findings that polymorphisms in SLC23A1/2 genes influenced ascorbate concentration in aqueous humor and lens nucleus.