Hostname: page-component-7c8c6479df-5xszh Total loading time: 0 Render date: 2024-03-18T11:38:52.126Z Has data issue: false hasContentIssue false

The distribution of ascorbic acid between various cellular components of blood, in normal individuals, and its relation to the plasma concentration

Published online by Cambridge University Press:  04 June 2009

Richard M. Evans
Affiliation:
Department of Clinical Biochemistry andHairmyres Hospital, East Kilbride, Lanarkshire, G75 8RG
Lilias Currie
Affiliation:
Department of Clinical Biochemistry andHairmyres Hospital, East Kilbride, Lanarkshire, G75 8RG
Allan Campbell
Affiliation:
Department of Medicine, Hairmyres Hospital, East Kilbride, Lanarkshire, G75 8RG
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. A study was undertaken to investigate the distribution of ascorbic acid between various cellular components of blood, in normal individuals, and its relation to the plasma concentration. Forty-one unsupplemented individuals and sixteen supplemented (2 g/d for 5 d) individuals were studied.

2. Granulocytes, mononuclear leucocytes, platelets and erythrocytes were separated by differential sedimentation and centrifugation. Ascorbic acid contents were measured by the dinitrophenylhydrazine method.

3. Ascorbic acid content per cel was higher in mononuclear leucocytes and granulocytes than in platelets and erythrocytes. Intracellular ascorbic acid concentrations, calculated from published values for cell volumes, when compared with the plasma concentration showed a marked ability to concentrate ascorbic acid in mononuclear leucocytes (80 times), platelets (40 times) and granulocytes (25 times).

4. Erythrocytes showed little ability to concentrate ascorbic acid over the normal range of plasma concentration but because of their relative numbers they and the plasma fraction accounted for most of the blood-borne ascorbic acid (> 70%).

5. The ascorbic acid content of granulocytes, platelets and erylhrocytes showed a significant positive correlation with the plasma concentration and supplementation with ascorbic acid significantly increased the content of these cell types. Mononuclear leucocytes in contrast did not show any such relationship.

6. The ability of the mononuclear leucocytes to maintain the highest levels of ascorbic acid in the cell types studied, despite variation in plasma availability, warrants further study, particularly in view of the importance of these cells in immunocompetence.

Type
Papers of direct reference to Clinical and Human Nutrition
Copyright
Copyright © The Nutrition Society 1982

References

Barkhan, P. & Howard, A. N. (1958). Biochem J. 70, 163.CrossRefGoogle Scholar
Barton, G. M. G. & Roath, O. S. (1976). Int. J. Vitam. Nutr. Res. 46, 271.Google Scholar
Boyum, A. (1968). Scand. J. Clin. Lab. Invest. 21, Suppl. 77.Google Scholar
Cameron, E. & Campbell, A. (1974). Chem. Biol. Interact. 9, 285.CrossRefGoogle Scholar
Campbell, A. (1980). Chem. Biol. Interact. 30, 305.CrossRefGoogle Scholar
Campbell, A. & Jack, T. (1979). Scott. Med. J. 24, 151.CrossRefGoogle Scholar
Davidsohn, I. & Nelson, D. A. (1974). In Clinical Diagnosis by Laboratory Methods, p. 123 [Davidsohn, I. and Henry, J. B., editors]. London: W. B. Saunders.Google Scholar
Denson, K. W. & Bowers, E. F. (1961). Clin. Sci. 21, 157.Google Scholar
Evans, R. M., Currie, L. & Campbell, A. (1980). Ann. Clin. Biochem. 17, 252.CrossRefGoogle Scholar
Gibson, S. L. M., Moore, F. M. L. & Goldberg, A. (1966). Br. Med. J. i, 1152.CrossRefGoogle Scholar
Griffiths, L. L., Brocklehurst, J. C., Scott, D. L., Marks, J. & Blackley, J. (1967). Geront. Clin. 9, 1.CrossRefGoogle Scholar
Horrobin, D. F., Manku, M. S., Oka, M., Morgan, R. O., Cunnane, S. C., Ally, A. I., Ghayur, T., Schweitzer, M. & Karmali, R. A. (1979). Med. Hypotheses 5, 969.CrossRefGoogle Scholar
Horrobin, D. F., Oka, M. & Manku, M. S. (1979). Med. Hypotheses 5, 849.CrossRefGoogle Scholar
Hume, R. & Weyers, E. (1973). Scott. Med. J. 18, 3.CrossRefGoogle Scholar
Leibovitz, B. & Siegel, B. V. (1978). Int. J. Vitam. Nutr. Res. 48, 159.Google Scholar
Lewin, S. (1976). Vitamin C: Its Molecular Biology and Medical Potential. London: Academic Press.Google Scholar
Lloyd, J. V., Davis, P. S., Emery, H. & Lander, H. (1972). J. Clin. Path. 25, 478.CrossRefGoogle Scholar
Loh, H. S. & Wilson, C. W. M. (1971 a). Br. Med. J. iii, 733.CrossRefGoogle Scholar
Loh, H. S. & Wilson, C. W. M. (1971 b). Int. J. Vitam. Nutr. Res. 41, 90.Google Scholar
Lowry, O. H., Bessey, O. A., Brock, M. J. & Lopez, J. A. (1946). J. biol. Chem. 166, 111.CrossRefGoogle Scholar
MacLennan, W. J. & Hamilton, J. C. (1976). Age Ageing 5, 43.CrossRefGoogle Scholar
Manku, M. S., Oka, M. & Horrobin, D. F. (1979). Prostaglandins Med. 3, 129.CrossRefGoogle Scholar
Murata, A. (1975). Proc. 1st int. Cong. Microbiol. Soc. Sci. Counc. Jap. 3, 432.Google Scholar
Prinz, W., Bortz, R., Bregin, B. & Hersch, M. (1977). Int. J. Vitam. Nutr. Res. 47, 248.Google Scholar
Sahud, M. A. & Aggeler, P. M. (1970). Proc. Soc. exp. Biol. 134, 13.CrossRefGoogle Scholar
Tivey, H., Li, J. G. & Osgood, E. E. (1951). Blood 6, 1013.CrossRefGoogle Scholar
Vallance, B. D., Hume, R. & Weyers, E. (1978). Br. Heart J. 40, 64.CrossRefGoogle Scholar
Vallance, S. (1977). Br. med. J. ii, 437.CrossRefGoogle Scholar
Wilson, P. A., McNicol, G. P. & Douglas, A. S. (1967). Lancet i, 975.CrossRefGoogle Scholar
Yonemoto, R. H., Chretien, P. B. & Fehniger, T. F. (1976). Proc. Am. Ass. Cancer Res. 17, 288.Google Scholar