Hostname: page-component-586b7cd67f-gb8f7 Total loading time: 0 Render date: 2024-11-30T04:36:30.727Z Has data issue: false hasContentIssue false

The effect of siderosis and ascorbic acid depletion on bone metabolism, with special reference to osteoporosis in the Bantu

Published online by Cambridge University Press:  06 August 2007

A. A. Wapnick
Affiliation:
South African MRC Iron and Red Cell Metabolism UnitDepartment of Medicine, University of the Witwatersrand, Johannesburg, South Africa
S. R. Lynch
Affiliation:
South African MRC Iron and Red Cell Metabolism UnitDepartment of Medicine, University of the Witwatersrand, Johannesburg, South Africa
H. C. Seftel
Affiliation:
South African MRC Iron and Red Cell Metabolism UnitDepartment of Medicine, University of the Witwatersrand, Johannesburg, South Africa
R. W. Charlton
Affiliation:
South African MRC Iron and Red Cell Metabolism UnitDepartment of Medicine, University of the Witwatersrand, Johannesburg, South Africa
T. H. Bothwell
Affiliation:
South African MRC Iron and Red Cell Metabolism UnitDepartment of Medicine, University of the Witwatersrand, Johannesburg, South Africa
Jenifer Jowsey
Affiliation:
Section of Surgical Research (Orthopedics), Mayo Clinic, and Mayo Foundation, Rochester, Minnesota, USA
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. There is an association between iron overload, ascorbic acid deficiency and osteoporosis in middle-aged South African Bantu males. The iron overload contributes to the ascorbic acid deficiency by accelerating its oxidative catabolism. The object of the present investigation was to explore the possibility that the osteoporosis results from chronic ascorbic acid deficiency.

2. On quantitative microradiography, percentage bone-formation surface was normal but percentage bone-resorption surface was significantly increased in ten osteoporotic subjects compared with seven control subjects.

3. There was a significant inverse correlation between bone mineral density and liver storage iron concentration in thirty-five Bantu subjects. In thirteen individuals aged 39 years or less, liver storage iron concentration was significantly correlated with percentage bone-resorption surface.

4. Guinea-pigs deprived of ascorbic acid for 21 d exhibited both significantly diminished percentage bone-formation surface and increased percentage bone-resorption surface.

5. Guinea-pigs overloaded with iron by injections of iron dextran developed significantly reduced hepatic ascorbic acid concentrations and bone mineral densities; percentage bone-formation surface was significantly diminished and percentage bone-resorption surface significantly increased. Ascorbic acid injection largely prevented the bone changes.

Type
Research Article
Copyright
Copyright © The Nutrition Society 1971

References

Albright, F. & Reifenstein, E. C. (1948). The parathyroid glands & metabolic bone disease. Baltimore: Williams and wilkins.Google Scholar
Arnold, J. S. (1964). In Dynamic studies of metabolic bone disease p. 59 [Pearson, O. H. and Joplin, G. F, editors].Oxford: Blackwell.Google Scholar
Bothwell, T. H.,Charlton, R. W. & Seftel, H. C. (1965). S. Afr. med. J. 39, 892.Google Scholar
Bothwell, T. H., Seftel, H., Jacobs, P., Torrance, J. D. & Baumslag, N. (1964). Am. J. clin. Nutr. 14, 47.CrossRefGoogle Scholar
Bourne, G. H. (1942). Lancet ii, 661.CrossRefGoogle Scholar
Bourne, G. (19421943). J. Physiol., Lond. 101, 327.CrossRefGoogle Scholar
Bourne, G. H. (19431944). J. Physiol., Lond. 102, 319.CrossRefGoogle Scholar
Dalldorf, G. (1938). J. Am. med. Ass. III, 1376.CrossRefGoogle Scholar
Follis, R. H. Jr (1951). Bull. Johns Hopkins Hosp. 89, 9.Google Scholar
Friberg, U. & Ringertz, N. R. (1954). Expl Cell Res. 6, 527.CrossRefGoogle Scholar
Gould, B. S. (1963). Int. Rev. Cytol. 15, 301.Google Scholar
Gould, B. S. & Shwachman, H. (19411942).Am. J. Physiol. 135, 485.CrossRefGoogle Scholar
Grusin, H. &Samuel, E. (1957). Am. J. Clin. Nutr. 5, 644.Google Scholar
Höjer, J. A. (1923). Acta paediat., Stockh. Suppl. no. 3, p. 48.Google Scholar
Jowsey, J. (1966). Am. J. Med. 40, 485.CrossRefGoogle Scholar
Lynch, S. R., Berelowitz, I., Seftel, H. C., Miller, G. B., Krawitz, P., Charlton, R. W. & Bothwell, T. H. (1967). Am. J. Clin. Nutr. 20, 799.Google Scholar
Lynch, S. R., Seftel, H. C., Torrance, J. D., Charlton, R. W. & Bothwell, T. H. (1967). Am. J. Clin. Nutr. 20, 641.Google Scholar
Lynch, S. R., Wapnick, A. A., Seftel, H. C., Charlton, R. W. & Bothwell, T. H. (1970). S. Afr. J. Med. Sci. 35, 45.Google Scholar
Maclean, D. L., Sheppard, M. & McHenry, E. W. (1939). Br. J. exp. Path. 20, 451.Google Scholar
Mueller, K. H., Trias, A. & Ray, R. D. (1966). J. Bone Jt Surg. 48A, 140.CrossRefGoogle Scholar
Park, E. A., Guild, H. G., Jackson, D. & Bond, M. (1935). Archs Dis. Childh. 10, 265.Google Scholar
Roe, J. H. (1954). In Methods of biochemical analysis Vol. 1, p. 115 [Glick, D., editor]. New york: Interscience.CrossRefGoogle Scholar
Saville, P. D. (1965). J. Bone Jt Surg. 47A, 492.CrossRefGoogle Scholar
Seftel, H. C., Malkin, C., Schmaman, A., Abrahams, C., Lynch, S. R., Charlton, R. W. & Bothwell, T. H. (1966). Br. Med. J. i, 642.Google Scholar
Torrance, J. D. & Bothwell, T. H. (1968). S. Afr. J. med. Sci. 33, 9.Google Scholar
Trotter, M., Broman, G. E. & Peterson, R. R. (1960).J. Bone Jt Surg. 42A, 50.CrossRefGoogle Scholar
Trowell, H. C. (1960). Non-Infective disease in africa. London: Edward arnold.Google Scholar
Walker, A. R. P. & Arvidsson, U. B. (1953). Trans. R. Soc. trop. Med. Hyg. 47, 536.CrossRefGoogle Scholar
Wapnick, A. A., Lynch, S. R., Krawitz, P., Seftel, H. C., Charlton, R. W. & Bothwell, T. H. (1968). Br. med. J. iii, 704.Google Scholar
williams, J. A. &Nicholson, G. I. (1963). Lancet i, 1408.CrossRefGoogle Scholar