Abstract
Kiwifruit are a rich source of vitamin C and also contain numerous phytochemicals, such as flavonoids, which may influence the bioavailability of kiwifruit-derived vitamin C. The aim of this study was to compare the relative bioavailability of synthetic versus kiwifruit-derived vitamin C using a randomised cross-over pharmacokinetic study design. Nine non-smoking males (aged 18–35 years) received either a chewable tablet (200 mg vitamin C) or the equivalent dose from gold kiwifruit (Actinidia chinensis var. Sungold). Fasting blood and urine were collected half hourly to hourly over the eight hours following intervention. The ascorbate content of the plasma and urine was determined using HPLC with electrochemical detection. Plasma ascorbate levels increased from 0.5 h after the intervention (P = 0.008). No significant differences in the plasma time-concentration curves were observed between the two interventions (P = 0.645). An estimate of the total increase in plasma ascorbate indicated complete uptake of the ingested vitamin C tablet and kiwifruit-derived vitamin C. There was an increase in urinary ascorbate excretion, relative to urinary creatinine, from two hours post intervention (P < 0.001). There was also a significant difference between the two interventions, with enhanced ascorbate excretion observed in the kiwifruit group (P = 0.016). Urinary excretion was calculated as ~40% and ~50% of the ingested dose from the vitamin C tablet and kiwifruit arms, respectively. Overall, our pharmacokinetic study has shown comparable relative bioavailability of kiwifruit-derived vitamin C and synthetic vitamin C.
Highlights
In contrast to most mammals, humans cannot synthesis vitamin C due to mutation of the terminal biosynthetic enzyme [1]
It has been proposed that food-derived flavonoids may “spare” vitamin C and increase its bioavailability
Nine participants with above average plasma ascorbate levels were enrolled for the study and provided written informed consent
Summary
In contrast to most mammals, humans cannot synthesis vitamin C (ascorbate) due to mutation of the terminal biosynthetic enzyme [1]. The micronutrient must be obtained from dietary sources in order to prevent hypovitaminosis C and the potentially fatal deficiency disease scurvy [1]. Vitamin C was first isolated from fruit and vegetables and the adrenal glands of animals in the early 1930s and was chemically synthesized in 1933 [2]. Synthetic and food-derived vitamin C is chemically identical, fruit and vegetables contain numerous nutrients and phytochemicals, e.g., flavonoids, which may affect the bioavailability of food-derived vitamin C. It has been proposed that food-derived flavonoids may “spare” vitamin C and increase its bioavailability
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