Vitamin C metabolism during infections

by Harri Hemilä

This text is based on pages 61-62 of Hemilä (2006).
This document has up to date links to documents that are available via the net.
Harri Hemilä
Department of Public Health
University of Helsinki,  Helsinki, Finland

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Version May 29, 2012

In guinea pigs, tuberculosis and other infections lead to a decrease in vitamin C concentration in the adrenals and urine (Abbasy et al. 1937a,b; Harris et al. 1937; Birkhaug 1938). In rats, Trypanosoma infection decreased the concentration of reduced vitamin C in spleen and adrenals, and increased the proportion of vitamin C in the oxidized dehydroascorbic acid form (Nyden 1948). In mice, influenza A infection resulted in a decrease in vitamin C concentration in bronchoalveolar lavage fluid, concomitant with an increase in dehydroascorbic acid (Buffinton et al. 1992). In macaque monkeys, malaria caused a reduced vitamin C level in plasma (McKee & Geiman 1946). In cows, intramammary infusion of E. coli (Weiss et al. 2004) and clinical mastitis (Kleczkowski et al. 2005) decreased plasma vitamin C concentration. Furthermore, bacterial toxins cause loss of vitamin C from many tissues (Harde 1934; Lyman & King 1936; Harris et al. 1937; Torrance 1940; Garcia et al. 1990; Rojas et al. 1996; Benito & Bosch 1997; Yamaguchi et al. 1997; Armour et al. 2001; Victor et al. 2002), but one study found an increase in vitamin C level in the livers of mice administered endotoxin (Jeffries 1965).

A large number of studies with human subjects found that vitamin C levels decrease in plasma, leucocytes and urine during various infections, including pneumonia and tuberculosis (Leppo 1939; Banerjee et al. 1940; Sweany et al. 1941; Sinha et al. 1984; Tanzer & Özalp 1993; Hunt et al. 1994; Galley et al. 1996, 1997; Pfitzenmeyer et al. 1997; Plit et al. 1998; Bakaev et al. 2004; for further refs., see Hemilä 1997a; Hemilä & Douglas 1999). Moreover, several reports noted that more severe forms of tuberculosis are more often associated with lower vitamin C levels than milder forms of the disease (Hemilä 1997a).

In the common cold infections, plasma, leukocyte and urine vitamin C levels decrease (Davies et al 1979; for refs., see Hemilä 1992a, 1997a). Hume and Weyers (1973) reported that vitamin C level in leukocytes was reduced to half when their subjects contracted a cold, but the level returned to the original level in about a week after the episode. Vitamin C supplementation (6 g/day) essentially abolished the fall in leukocyte vitamin C level caused by colds (Fig. 1).

Although low vitamin C levels in patients with infections may partly be explained by low dietary intakes, there are several studies in which the dietary intake of vitamin C was comparable between the patients and healthy controls, indicating that low dietary intake cannot be the only cause of low vitamin C levels in the patients with infections (Hemilä 1997a). Increased levels of dehydroascorbic acid have also been reported in patients with various infections, consistent with the notion that vitamin C may be oxidized during infections (Banerjee & Belavady 1953; Chakrabarti & Banerjee 1955).

Endotoxin administration reduced plasma vitamin C concentration in human subjects (Pleiner et al. 2002, 2003), and vitamin C supplementation abolished the exercise-induced increase in plasma endotoxin level (Ashton et al. 2003).

Fig. 1. The effect of the common cold infection on leucocyte vitamin C level.

Effect of the common cold on leukocyte vitamin C level
In 7 control participants, the vitamin C level in leucocytes (μg/108 cells) is indicated by triangles. Vitamin C level is indicated by squares in 3 vitamin C participants supplemented regularly with 1 g/day and, after the onset of the cold, with 6 g/day for 3 days, and thereafter with 1 g/day again. Day 0 indicates pre-cold level. The figure is based on tables I and III of Hume & Weyers (1973).


NOTE: All the links in the main text should be freely accessible at least as an abstract, but some links below require a permission from publisher for any access.

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Copyright: © 2006-2009  Harri Hemilä. This text is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.  

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