Ascorbate Influence on Function of Phagocytes

An essential step in phagocytosis involves travel of neutrophils to the site of infection through their adherence to the vessel wall and travel between endothelial cells (diapedesis). Jonas et al (1993) reported that ascorbate reduced neutrophil adhesion to endothelial cells and provided a protective effect this conclusion was not valid because the difference between ascorbate-treated and control groups was only 1%. In another report, on seven patients who had renal transplant (Thomer et al., 1983), ascorbate was shown to increase neutrophil adhesion. More studies with larger sample size are needed to elucidate further the role of ascorbate in adhesion. 

Physiological significance of in vitro studies utilizing millimolar amounts of ascorbate is supported by data from studies in humans, who cannot synthesize vitamin C, as well as in animals that can make their own ascorbate (Anderson, 1981a). In a small study of five healthy human subjects, Anderson et al. (1980) showed that the daily ingestion of 2-3 g sodium ascorbate for one week led to a 

Activated phagocytes can release superoxide anion into the extracellular fluid as well as leak it into the cytoplasm. Superoxide can give rise to hydrogen peroxide 

Furthermore, it has been shown (Anderson et aL, 1987 Anderson and Lukey, 1987) that ascorbate can mediate efficient neutralization of extracellular phagocyte-derived oxidants without affecting the formation of bactericidal oxygen radicals within the intracellular phagosome. This appears to be a major role of ascorbate in phagocytic cells. In addition, ascorbate was shown to protect rabbit macrophages in vitro from injuries associated with phagocytosis (McKee and Myrvik, 1979). 

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