Abstract

Plasma vitamin C concentrations fluctuate in response to recent dietary intake; therefore levels are typically determined in the fasting state. Erythrocyte ascorbate concentrations have been shown to be similar to plasma levels, but little is known about the kinetics of ascorbate accumulation in these cells. In this study, we investigated ascorbate uptake into erythrocytes after dietary supplementation with vitamin C and compared it to changes in plasma ascorbate concentrations. Seven individuals with baseline fasting plasma vitamin C concentrations ≥ 50 µmol/L were depleted of vitamin C-containing foods and drinks for one week, and then supplemented with 250 mg vitamin C/day in addition to resuming their normal diet. Fasting or steady-state plasma ascorbate concentrations declined to almost half of their baseline concentration over the week of vitamin C depletion, and then returned to saturation within two days of beginning supplementation. Erythrocyte ascorbate concentrations exhibited a very similar profile to plasma levels, with values ~76% of plasma, and a strong linear correlation (r = 0.89, p < 0.0001). Using a pharmacokinetic study design in six individuals with baseline fasting plasma vitamin C concentrations ≥50 µmol/L, we also showed that, unlike plasma, which peaked between 2 and 4 h following ingestion of 200 mg of vitamin C, erythrocyte ascorbate concentrations did not change in the six hours after supplementation. The data from these two intervention studies indicate that erythrocyte ascorbate concentration provides a stable measure of steady-state plasma ascorbate status and could be used to monitor ascorbate status in healthy non-fasting individuals.

Highlights

  • Humans, unlike most other animals, have lost the ability to synthesise vitamin C due to evolutionary conserved mutations in the gene encoding L-gulonolactone oxidase, which catalyses the final step in the biosynthetic pathway [1]

  • In our study of healthy individuals, we found that the ascorbate content of erythrocytes did not change following healthy individuals, we found that the ascorbate content of erythrocytes did not change following dietary intake of the vitamin, despite there being a transient peak observed in the plasma

  • Red cell ascorbate concentrations were ~0.76 of those of plasma, using the gradient of line. These findings suggest that erythrocyte ascorbate content could be used as an indicator of the the regression line. These findings suggest that erythrocyte ascorbate content could be used as an steady-state plasma ascorbate concentrations in non-fasting individuals, as this measurement does not indicator of the steady-state plasma ascorbate concentrations in non-fasting individuals, as this seem to be subject to transient fluctuations following dietary intake

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Summary

Introduction

Unlike most other animals, have lost the ability to synthesise vitamin C (ascorbate) due to evolutionary conserved mutations in the gene encoding L-gulonolactone oxidase, which catalyses the final step in the biosynthetic pathway [1]. Nutrients 2020, 12, 418 ascorbate concentrations < 23 μmol/L) has been described in up to 15% of individuals [4,5]. These levels are associated with early symptoms of scurvy, such as fatigue and depression [6]. Vitamin C is absorbed via the small intestine, released into the bloodstream and distributed to the tissues [7]. It is well recognised that the SVCTs are vital for ascorbate distribution in the body [10,11].

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