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The influence of Salmonella typhi-murium infection in rats on vitamin A metabolism*

Published online by Cambridge University Press:  15 May 2009

I. J. Kligler
Affiliation:
Department of Hygiene and Bacteriology, Hebrew University, Jerusalem
K. Guggenheim
Affiliation:
Department of Hygiene and Bacteriology, Hebrew University, Jerusalem
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Since Green & Mellanby (1928, 1930) reported that vitamin A protected the body against infection, this problem has been studied by various authors (Verder, 1928; Lassen, 1930, 1931; Seidmon & Arnold, 1931–2; Boynton & Bradford, 1931; McClung & Winters, 1932; Stryker & Janota, 1941). In general, the results showed that A avita-minotic animals were more susceptible to spontaneous or experimental infections than controls kept on a normal diet. However, in so far as we know, no experimental work has been done on the inverse problem—the effect of infection on vitamin A metabolism.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1945

References

REFERENCES

Baumann, C. A., Riising, R. M. & Steenbock, H. (1934). J. Biol. Chem. 107, 705.CrossRefGoogle Scholar
Boynton, L. C. & Bradford, W. L. (1931). J. Nutrit. 4, 323.CrossRefGoogle Scholar
De, N. K. (1937). Indian J. Med. Res. 24, 751.Google Scholar
Greaves, J. D. & Schmidt, C. L. A. (1935a). Amer. J. Physiol. 111, 492.CrossRefGoogle Scholar
Greaves, J. D. & Schmidt, C. L. A. (1935b). Amer. J. Physiol. 111, 502.CrossRefGoogle Scholar
Green, H. N. & Mellanby, E. (1928). Brit. Med. J. 2, 691.CrossRefGoogle Scholar
Green, H. N. & Mellanby, E. (1930). Brit. J. Path. 11, 81.Google Scholar
Guilbert, H. R. (1934). Industr. Engng Chem. (Anal. ed.), 6, 452.Google Scholar
Heymann, W. (1936). Amer. J. Die. Child. 51, 273.Google Scholar
Kemmerer, A. R. & Fraps, G. S. (1938). J. Nutrit. 16, 309.CrossRefGoogle Scholar
Kuhn, R. & Brockmann, H. (1932). Hoppe-Seyl. Z. 206, 41.CrossRefGoogle Scholar
Lassen, H. C. A. (1930). J. Hyg. 30, 300.CrossRefGoogle Scholar
Lassen, H. C. A. (1931). Z. Immunforsch. 73, 221.Google Scholar
Lindquist, T. (1938). Acta Med. Scand. Suppl. 97, 1.Google Scholar
McClung, L. S. & Winters, J. C. (1932). J. Infect. Dis. 51, 469.CrossRefGoogle Scholar
Monceaux, R. H. (1938a). Pr. méd. 46, 1183.Google Scholar
Monceaux, R. H. (1938b). J. Pharm. Chim., Paris, 28, 297.Google Scholar
Moore, T. (1931). Biochem. J. 25, 275.CrossRefGoogle Scholar
Peterson, W. J., Hughes, J. S. & Freeman, H. F. (1937). Industr. Engng Chem. (Anal. ed.), 9, 71.Google Scholar
Russell, W. C., Taylor, M. W., Walker, H. A. & Polskin, L. J. (1942). J. Nutrit. 24, 199.CrossRefGoogle Scholar
Seidmon, E. & Arnold, L. (1931-1932). Proc. Soc. Exp. Biol., N.Y., 29, 393.CrossRefGoogle Scholar
Stryker, W. A. & Janota, M. (1941). J. Infect. Dis. 69, 243.CrossRefGoogle Scholar
Verder, E. (1928). J. Infect. Dis. 42, 589.CrossRefGoogle Scholar