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Cited by 158

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

The non-oxidative degradation of ascorbic acid at physiological conditions

Open access
Simpson, Gregory L.W, Ortwerth, B.J·2000·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Abstract

The degradation of L-ascorbate (AsA) and its primary oxidation products, L-dehydroascorbate (DHA) and 2,3-L-diketogulonate (2, 3-DKG) were studied under physiological conditions. Analysis determined that L-erythrulose (ERU) and oxalate were the primary degradation products of ASA regardless of which compound was used as the starting material. The identification of ERU was determined by proton decoupled (13)C-nuclear magnetic resonance spectroscopy, and was quantified by high performance liquid chromatography, and enzymatic analysis. The molar yield of ERU from 2,3-DKG at pH 7.0 37 degrees C and limiting O(2)97%. This novel ketose product of AsA degradation, was additionally qualitatively identified by gas-liquid chromatography, and by thin layer chromatography. ERU is an extremely reactive ketose, which rapidly glycates and crosslinks proteins, and therefore may mediate the AsA-dependent modification of protein (ascorbylation) seen in vitro, and also proposed to occur in vivo in human lens during diabetic and age-onset cataract formation.

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Metadata

Authors
Simpson, G. L. W., & Ortwerth, B. J.
Venue
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher
Elsevier BV
Published
2000-04
Volume
1501
Issue
1
Pages
12-24
ISSN
0925-4439 (ISSN-L)
OpenAlex
W2079021848
Cited by
158
References
2
FWCI
4.18
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: The non-oxidative degradation of ascorbic acid at physiological conditions. https://app.cochat.ai/papers/10.1016/s0925-4439(00)00009-0
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Simpson, G. L. W., & Ortwerth, B. J. (2000). The non-oxidative degradation of ascorbic acid at physiological conditions. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. https://doi.org/10.1016/s0925-4439(00)00009-0

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