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Plasma amino acids and tissue methionine levels in fruit bats (Rousettus aegyptiacus) with nitrous oxide-induced vitamin B12 deficiency

Published online by Cambridge University Press:  24 July 2007

Justin Van Der Westhuyzen ,
Suasn V. Van Tonder ,
Jayne E. Gibson ,
Terence A. Kilroe-smith  and
Jack Metz
Justin Van Der Westhuyzen
Affiliation:
Department of Haematology, School of Pathology of the South African Institute for Medical Research, and the University of the Witwatersrand, POBox 1038, Johannesburg 2000, South Africa
Suasn V. Van Tonder
Affiliation:
Department of Haematology, School of Pathology of the South African Institute for Medical Research, and the University of the Witwatersrand, POBox 1038, Johannesburg 2000, South Africa
Jayne E. Gibson
Affiliation:
Department of Haematology, School of Pathology of the South African Institute for Medical Research, and the University of the Witwatersrand, POBox 1038, Johannesburg 2000, South Africa
Terence A. Kilroe-smith
Affiliation:
National Centre for Occupational Health, Johannesburg, South Africa
Jack Metz
Affiliation:
Department of Haematology, School of Pathology of the South African Institute for Medical Research, and the University of the Witwatersrand, POBox 1038, Johannesburg 2000, South Africa
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Abstract

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1. The effect of methylcobalamin inactivation by the gas nitrous oxide on plasma amino acid and tissue methionine levels in fruit bats (Rousettus aegyptiacus) was examined.

2. Animals exposed to N2O-oxygen (1:1, v/v) for 90 min daily received a fruit diet with or without methionine or betaine supplements. Exposure and diets were continued for up to 17 weeks or until neurological impairment and muscular weakness was established.

3. All the groups exposed to N2O had significantly lower liver, brain and plasma methionine concentrations except the methionine-supplemented animals which showed significantly raised levels. Plasma homocysteine, which was absent in controls, was present in all the N2O-exposed groups.

4. Betaine supplementation resulted in reduced accumulation of homocysteine in plasma. However, plasma and liver methionine levels were only slightly increased compared with animals on the basal diet, and brain methionine levels were the lowest of all the groups studied.

5. These results support the hypothesis that reduced methionine synthesis is an important contributor to the development of neurological impairment in this species and suggest that dietary supplementation with the methionine precursor betaine cannot replace the loss of vitamin B12-dependent methionine synthesis.

Type
Papers on General Nutrition
Information
British Journal of Nutrition , Volume 53 , Issue 3 , May 1985 , pp. 657 - 662
Copyright
Copyright © The Nutrition Society 1985

References

Banks, R. G. S., Henderson, R. J. & Pratt, J. M. (1968). Journal of the Chemical Society (A), 2886–2889.CrossRefGoogle Scholar
Chanarin, I. (1980). In Vitamins in Medicine, vol. 1, pp. 172–246 [Barker, B. M. and Bender, D. A. editors]. London: Heinemann Medical Books.Google Scholar
Chanarin, I., Deacon, R., Lumb, M. & Perry, J. (1980). Lancet ii, 505–508.CrossRefGoogle Scholar
Das, K. C. & Herbert, V. (1976). Clinics in Haematology 5, 697–725.CrossRefGoogle Scholar
Deacon, R., Jennings, P., Lumb, M., Perry, J., Purkiss, P. & Chanarin, I. (1981). Scandinavian Journal of Haematology 27, 267–270.CrossRefGoogle Scholar
Deacon, R., Lumb, M., Perry, J., Chanarin, I., Minty, B., Halsey, M. J. & Nunn, J. F. (1978). Lancet, ii, 1023–1024.CrossRefGoogle Scholar
Deacon, R., Lumb, M., Perry, J., Chanarin, I., Minty, B., Halsey, M. J. & Nunn, J. F. (1980). European Journal of Biochemistry 104, 419–422.CrossRefGoogle Scholar
Fürst, P. (1983). Proceedings of the Nutrition Society 42, 451–462.CrossRefGoogle Scholar
Kondo, H., Osborne, M. L., Kolhouse, J. F., Binder, M. J., Podell, E. R., Utley, C. S., Abrams, R. S. & Allen, R. H. (1981). Journal of Clinical Investigation 67, 1270–1283.CrossRefGoogle Scholar
Lee, P. L. Y. (1974). Biochemical Medicine 10, 107–121.CrossRefGoogle Scholar
Lumb, M., Sharer, N., Deacon, R., Jennings, P., Purkiss, P., Perry, J. & Chanarin, I. (1983). Biochimica et Biophysica Acta 756, 354–359.CrossRefGoogle Scholar
Peck, E. J. & Awapara, J. (1967). Biochimica et Biophysica Acta 141, 499–506.CrossRefGoogle Scholar
Scott, J. M., Dinn, J., Wilson, P. & Weir, D. G. (1981). Lancet ii, 334–337.CrossRefGoogle Scholar
Sturman, J. A., Gaull, G. E. & Niemann, W. H. (1976). Journal of Neurochemistry 27, 425–431.CrossRefGoogle Scholar
van der Westhuyzen, J., Cantrill, R. C., Fernandes-Costa, F. & Metz, J. (1983). Journal of Nutrition 113, 531–537.CrossRefGoogle Scholar
van der Westhuyzen, J., Fernandes-Costa, F. & Metz, J. (1982). Life Sciences 31, 2001–2010.CrossRefGoogle Scholar
van der Westhuyzen, J. & Metz, J. (1984). Journal of Nutrition 114, 1106–1111.CrossRefGoogle Scholar