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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #107897
Title: MARGINAL DIETARY PYRIDOXINE AND SUPPLEMENTAL DIETARY HOMOCYSTINE AFFECT THE RESPONSE OF THE RAT TO NICKEL DEPRIVATION

Author
item Nielsen, Forrest - Frosty
item Yokoi, Katsuhiko
item Uthus, Eric

Submitted to: International Symposium on Metal Ions in Biology and Medicine
Publication Type: Abstract Only
Publication Acceptance Date: 1/7/2000
Publication Date: 5/7/2000
Citation: Nielsen, F.H., Yokoi, K., Uthus, E.O. 2000. Marginal dietary pyridoxine and supplemental dietary homocystine affect the response of the rat to nickel deprivation [abstract]. 6th International Symposium on Metal Ions in Biology and Medicine Scientific Program and Book of Abstracts, San Juan, Puerto Rico, May 7-10, 2000, p.202.

Interpretive Summary:

Technical Abstract: An experiment was conducted to ascertain whether the reduced form of homocysteine, or homocystine (Hcy), and the in vivo precursor of homocysteine, methionine (Met), could be used as dietary stressors to enhance or alter the signs of nickel deprivation and thereby provide clues as to the biochemical function of nickel in higher animals. Because B6 is important in the metabolism of homocysteine, it was also included as a dietary stressor. The experiment was 2 x 2 x 3 factorially arranged with nickel supplemented at 0 and 1 mg/kg diet, B6 supplemented at 0 and 7.5 mg/kg and dietary amino acid supplements of none, 10 g/kg Hcy and 10 g/kg Met. The basal diet contained about 8 ng of nickel, 1.8 mg of B6 and 4.7 g of Met per kg. Nickel deprivation increased urine volume and urinary nitrate excretion during a 20-hour collection period. Hcy supplementation decreased urinary nitrate excretion which seemed to decrease the nickel effect. Both alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were decreased by Hcy and Met supplementation in nickel-deficient rats, but increased in nickel-supplemented rats. B6 deficiency decreased both ALT and AST regardless of dietary nickel and amino acid supplementation. Triglycerides were increased by Hcy and Met in nickel-deficient rats, in nickel-supplemented rats Hcy and Met induced a small decrease. The findings indicate that met and hcy supplementation and B6 deficiency affect the response to nickel deprivation, and suggest that nickel has a biological role that may not be directly involved, but can affect the metabolism of sulfur amino acids.