Magnesium Deficiency and Urea Cycle Enzymes in Rat Liver.* (32414)

Journal/Book: Reprinted from PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOCY AND MEDICINE 1967 v126 249-251. 1967;

Abstract: Department of Medicine West Virginia University Medical Center Morgantown * Supported in part by USPHS Grant NBO 3152. Â† Trainee of USPHS (5-T1-AM-5381-04). Induction of magnesium deficiency in the rat has been observed to produce several metabolic abnormalities. Recently we have reported a generalized aminoaciduria in the presence of an increase in the activity of sodium-potassium activated kidney adenosine triphosphatase and the suggestion was made that the alteration in the urinary amino acid pattern was the result of renal tubular dysfunction rather than an "overflow of amino-aciduria" (1) . Since protein metabolism was altered in the deficient animals it seemed appropriate to study the influence of magnesium deficiency an the urea cycle enzymes. These enzymes have been shown to undergo adaptative changes whenever dietary protein intake is quantitatively changed (2 3). The activity of the enzymes has been altered by adrenalectomy(4) growth hormone administration (5) or treatment with ethionine (6) carbon tetrachloride(7) or azo dyes(8). In all of these experimental designs protein metabolism was affected either directly by stimulating catabolic or anabolic processes or indirectly by producing hormone imbalances with their concomitant alterations in general metabolic processes. Materials and methods. Albino female rats (Holtzman) of initial weight of 150-200 g were divided into control and deficient groups. The magnesium deficient diet (General Biochemicals Chagrin Falls Ohio) was homogenized in water and each rat was given 7.5 g of the diet twice daily by gavage feeding; one milliequivalent of magnesium acetate was added to each feeding in the control rats. The diet was analyzed for magnesium content by methods previously reported (1) and with results as follows: control diet 2.0165 mEq/ 15 g; deficient diet 0.0165 mEq/15 g. At the end of 30 days the animals were sacrificed by exsanguination and the livers were quickly removed weighed and homagenized in the ratio of 1 g of liver to 9 ml of 0.1 % cetyltrimethyl ammonium bromide using a Potter-Elvehjem glass homogenizer and a motor driven pestle. The homogenates were then centrifuged at 4000 õ g for 15 minutes at 5°C and the clear supernate assayed for carbamyl phosphate synthetase ornithine transcarbamylase arginasuccinte synthetase argininosuccinase and arginase by the method of Brown and Cohen (9) . The results of the enzyme assays are expressed as micromoles of product farmed per hour per g of liver. ... ___MH

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