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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 #86996


item Uthus, Eric
item Poellot, Rhonda Lee

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 4/18/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Previous studies indicate that arsenic (As) has a physiological role affecting methionine metabolism, possibly by affecting methionine recycling. Thus, a study was designed to determine the effect of altering the dietary methionine (Meth) to cystine (Cys) ratio on As deprivation and excess. Male, weanling Sprague-Dawley rats were fed an amino acid-casein based diet containing <10 ng As/g. The experiment was a 3x2 design with dietary variables of As, as NaAsO2 (0, 0.5 or 50 ug As/g) and Meth/Cys molar ratio (5.76 or 0.37 [based on 1/2 Cys]). Because there was little effect of amino acid treatment on the parameters studied, these groups were combined in the statistical analysis. After about 10 weeks, growth tended (p<0.07) to be decreased in rats fed no supplemental As (0As) and in rats fed 50 ug As/g (50As) compared to rats fed 0.5 ug As/g (0.5As). Dietary arsenic had no effect on plasma cholesterol or kidney wt/body wt ratio. Blood urea nitrogen tended (p<0.08) to be increased in 50As. The activity of plasma ceruloplasmin was decreased (~2x) in 50As. Kidney iron and zinc concentrations were not affected by dietary As and the concentration of calcium tended (p<0.09) to be increased by 50As. In 50As, compared to either 0As or 0.5As, the kidney concentration of molybdenum was significantly increased, copper (Cu) was markedly increased (~10x), and magnesium (Mg) was increased ~2x. The effect of high dietary As on kidney Cu has been noted (Schmolke, et al, Hum Exp Toxicol, 1992, 11:315). The mechanism for accumulation of Cu and Mg is unknown but apparently it is not the result of metallothionein induction.