THE INFLUENCE OF DIET UPON NECROSIS CAUSED BY HEPATIC AND RENAL POISONS : PART II. DIET AND THE NEPHRITIS CAUSED BY POTASSIUM CHROMATE, URANIUM NITRATE, OR CHLOROFORM.

Abstract

Diet exerts a profound influence upon the toxicity (tested in the omnivorous white rat) of certain substances, namely, chloroform, phosphorus, potassium chromate, and uranium nitrate, which cause necrosis of the parenchymatous cells of the liver or of the kidney. Susceptibility to intoxication with all of these substances is less after a diet rich in carbohydrate than after a diet consisting of meat. Carbohydrates protect the parenchymatous cells of the liver or of the kidneys from necrosis caused by any one of these substances. Chloroform is much more toxic to animals which have received a diet consisting in great part of fat than to those which have received meat. When fat is fed to the white rat fatty infiltration occurs in the centers of the hepatic lobules and in the loops of Henle of the kidney. The necrosis caused by chloroform has the same location. The solubility of chloroform in fat determines the increased susceptibility of animals which have received fat and stored it in the parenchymatous cells of the liver and kidney. Susceptibility to intoxication with phosphorus which causes fatty degeneration and necrosis of the liver is not increased by a diet of fat. Necrosis caused by phosphorus occurs in the periphery of the hepatic lobule and exhibits maximum intensity in animals which have received meat. Susceptibility to intoxication with potassium chromate which causes nephritis with necrosis of the convoluted tubules of the kidney is not greater after a diet of fat than after a diet of meat. Susceptibility to intoxication with uranium nitrate which causes nephritis with advanced necrosis of renal tubules is increased by a diet of fat. The loops of Henle, in which fat is abundant after a diet of fat, are the chief site of necrosis.

• Authors: E L Opie, L B Alford
• Journal: The Journal of experimental medicine (J Exp Med) Vol. 21 Issue 1 Pg. 21-37 (Jan 01 1915) ISSN: 0022-1007 [Print] United States
• PMID: 19867849 (Publication Type: Journal Article)