Abstract

Ascorbate functions as an electron donor and scavenges free radicals. Dehydroascorbic acid (DHA), the oxidized form of ascorbate, is generated as a result of these reactions. While low plasma ascorbate levels have been reported in hemodialysis patients worldwide, no studies have measured DHA because it is not generalized. In this study, we aimed to clarify whether plasma ascorbate levels are low in dialysis patients and whether plasma ascorbate levels fluctuate before and after dialysis. Moreover, we applied our previously established method to measure the plasma ascorbate and DHA levels in chronic kidney disease (CKD) stage G3–G5 non-hemodialysis-dependent patients, and pre- and post-dialysis plasma ascorbate and DHA levels in CKD stage G5D hemodialysis patients. The sample size was calculated using G-power software. The pre-dialysis plasma total ascorbate levels, including DHA, were significantly (56%) lower in hemodialysis patients than in non-hemodialysis-dependent CKD patients. After dialysis, there was a 40% reduction in the plasma total ascorbate levels. Hemodialysis increased the post-dialysis plasma proportions of DHA from 37% to 55%. The study results demonstrated lower plasma total ascorbate levels in hemodialysis patients compared with in non-hemodialysis-dependent CKD patients; these low levels in hemodialysis patients were further reduced by hemodialysis and increased DHA proportion.

Highlights

  • Vitamin C (L-ascorbic acid) is a water-soluble micronutrient and antioxidant that scavenges reactive oxygen species, such as superoxide and hydroxyl radicals [1,2,3]

  • We examined whether dialysis reduced plasma ascorbate and Dehydroascorbic acid (DHA) levels and the percentage of DHA per total ascorbic acid, including DHA

  • We found that plasma total ascorbate, ascorbate, and DHA levels in hemodialysis patients tended to correlate with plasma potassium levels

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Summary

Introduction

Vitamin C (L-ascorbic acid) is a water-soluble micronutrient and antioxidant that scavenges reactive oxygen species, such as superoxide and hydroxyl radicals [1,2,3]. In addition to its antioxidant property, ascorbate contributes to numerous well-defined enzymatic reactions, involving collagen hydroxylation, norepinephrine biosynthesis, tyrosine metabolism, and peptide hormone amidation [5,6,7]. Dehydroascorbic acid (DHA), an oxidized form of ascorbic acid, is generated as a result of these reactions, and an increase in the DHA proportion suggests that the oxidative stress levels in vivo may be increasing [8]. Primates, including humans, cannot synthesize ascorbate because they carry multiple mutations in the Gulo gene encoding L-gulono-γ-lactone oxidase, the last enzyme in the ascorbate biosynthesis pathway [10]. Scurvy is a condition resulting from insufficient ascorbate in the body. Most scurvy symptoms, including anemia, weakness, and gingival bleeding, often occur in hemodialysis patients [11]

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