Hostname: page-component-76fb5796d-dfsvx Total loading time: 0 Render date: 2024-04-28T20:25:20.828Z Has data issue: false hasContentIssue false
  • English
  • Français

The Effects of Excessive Intake of Magnesium by the Rat; Especially concerning the Factors Relating to the Production of Renal Calculi

Published online by Cambridge University Press:  15 May 2009

Elsie Watchorn
Elsie Watchorn*
Affiliation:
From theBiochemical Laboratory, Cambridge.
*
1 Working with a full time personal grant from the Medical Research Council.
Rights & Permissions [Opens in a new window]

Extract

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. Rats taken from mixed stock diet and fed synthetic diet containing an excess of magnesium carbonate developed urinary calculi in a large number of cases.

2. The incidence of calculi was much higher in the females.

3. Addition of excess of calcium carbonate to the diet prevented the formation of calculi.

4. Rats previously fed for a short time on the synthetic diet and normal salt mixture did not develop calculi, but suffered from severe catharsis.

5. Rats on mixed stock diet had a more acid caecum and colon than those on synthetic diet.

6. No significant alterations were found in the Ca, Mg or inorganic P of the blood on any of the diets.

7. Extra magnesium, or calcium, or sodium carbonate lowered the urinary phosphate excretion.

8. Extra magnesium or calcium had little effect upon the urinary excretion of the other, but tended in each case to lower the output.

9. Changes in the sex organs brought about by excessive intake of magnesium are described.

The writer wishes to thank Miss V. E. Leader for her watchful care of the rats.

Type
Research Article
Information
Journal of Hygiene , Volume 32 , Issue 2 , April 1932 , pp. 156 - 170
Copyright
Copyright © Cambridge University Press 1932

References

REFERENCES

Abrahamson, and Miller, (1924–5). Proc. Soc. Exp. Biol. and Med. 22, 438.CrossRefGoogle Scholar
Bell, and Doisy, (1920). J. Biol. Chem. 44, 55.CrossRefGoogle Scholar
Elmslie, and Steenbock, (1929). J. Biol. Chem. 82, 611.CrossRefGoogle Scholar
Haag, and Palmer, (1928). J. Biol. Chem. 76, 367.CrossRefGoogle Scholar
Hart, and Steenbock, (1913). J. Biol. Chem. 14, 75.CrossRefGoogle Scholar
Huffman, , Robinson, , Winter, , and Larson, (1929–1930). J. Nutrition, 2, 471.CrossRefGoogle Scholar
Malcolm, (1905). J. Physiol. 32, 183.CrossRefGoogle Scholar
McCarrison, (1926–1927). Ind. J. Med. Res. 14, 895.Google Scholar
McCarrison, (1927–1928). Ind. J. Med. Res. 15, 197.Google Scholar
McCarrison, (1929–1930). Ind. J. Med. Res. 17, 1101.Google Scholar
McCollum, and Davis, (1915). J. Biol. Chem. 20, 641.CrossRefGoogle Scholar
McRobert, (1928–1929). Ind. J. Med. Res. 16, 545.Google Scholar
Meigs, Blatherwick and Cary, (1919). J. Biol. Chem. 40, 469.CrossRefGoogle Scholar
Mendel, and Benedict, (1909). Amer. J. Physiol. 25, 23.CrossRefGoogle Scholar
Newcomb, and Ranganathan, (1929–1930). Ind. J. Med. Res. 17, 1055.Google Scholar
Orr, , Holt, , Wilkins, and Boone, (1924). Amer. J. Dis. Child. 28, 574.Google Scholar
Osborne, and Mendel, (1917). J. Amer. Med. Assoc. 69, 32.CrossRefGoogle Scholar
Palmer, Eckles and Schutte, (1928–1929). Proc. Soc. Exp. Biol. and Med. 26, 58.CrossRefGoogle Scholar
Pribyl, (1929). C.R. Soc. Biol. 102, 258.Google Scholar
Ranganathan, (1930–1931). Ind. J. Med. Res. 18, 599.Google Scholar
Redman, Willimott and Wokes, (1927). Biochem. J. 21, 589.CrossRefGoogle Scholar
Richter-Quittner, (1924). C.R. Soc. Biol. 91, 596.Google Scholar
Shohl, and Pedley, (1922). J. Biol. Chem. 50, 537.CrossRefGoogle Scholar
Watchorn, (1926). Brit. J. Exp. Path. 7, 120.Google Scholar
Whelan, (1925). J. Biol. Chem. 63, 585.CrossRefGoogle Scholar
Zucker, and Matzner, (1923–1924). Proc. Soc. Exp. Biol. and Med. 21, 186.CrossRefGoogle Scholar