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Molybdenum liver content

Xanthine oxidase, which is capable of catalyzing the conversion of hypoxanthine and xanthine to uric acid, was first detected in 1882 by Horbaczewski (Hll), who noted that extracts of various tissues could catalyze the conversion of xanthine to uric acid. A similar enzyme was detected in milk (M15). These enzymes contain a flavin-adenine dinucleotide prosthetic group (C9). As a result of the essential nature of the flavin-adenine dinucleotide portion of the enzjmie, a striking parallelism was seen between the riboflavin content of the diet and the xanthine oxidase concentration in tissues of growing rats (DIO). The enzyme contains molybdenum. That the molybdenum is contained in a functionally important component has been demonstrated by several workers (G13, T5). Totter and his associates injected labeled molybdate into a cow, and then isolated the enzyme from the milk to show that the proportion between the molybdenum and flavin remained constant at a value of 0.5. Corran et al. (C9) postulated that the xanthine oxidase of milk is identical with the xanthine oxidase of liver, but the protein portions of the enzyme appear to differ. [Pg.170]

Although trace element abnormalities occur in chronic renal failure, few symptoms have been attributed to them in nondialyzed patients. In dialysis patients these disturbances appear to be qualitatively similar but more severe (T7). They have been extensively reviewed by Alfrey (A5). Total body zinc (except in erythrocytes), strontium, aluminum, and tin are generally increased, whereas total body rubidium is decreased. Iron stores tend to be increased in the spleen and liver in dialyzed patients, especially after ferrous sulfate therapy. Copper is increased in lung tissue and decreased in heart tissue and erythrocytes. Molybdenum and cadmium are decreased in renal tissue but increased in liver tissue of dialyzed and nondialyzed patients. Total body zinc content is significantly increased (A5), but hypozincemia, frequently observed in dialysis patients, has been blamed for taste impairment and impotence and there is conflicting evidence on whether zinc repletion corrects these abnormalities (K4, Ml2). Nickel is also increased in the serum of uremic patients, but this does not appear to be associated with a corresponding increase in tissues (S5). It cannot be concluded that trace element retention in renal failure is of no clinical importance, as shown by the problem of aluminum intoxication, to be discussed later. In addition, trace elements such as rubidium and bromine, which are rapidly depleted in uremic patients on maintenance dialysis (A5), may prove to be essential in normal metabolism. Thus the clinical importance of these element alterations remains unclear. [Pg.65]

Ruminants are quite susceptible to copper toxicity. These are the only animals in which significant, and even lethal, copper toxicity can occur without an inherited abnormality or the addition of dietary copper supplements. Copper toxicity may develop in sheep taking forage with a normal copper content of 8-10 mg kg and this is even more likely to occur if the molybdenum concentration in the diet is below 0.5 mg kg k The principal effects are on the liver and blood, with fatal hepatitis or hemolytic anemia occurring (Howell 1991a). In these respects, cattle are much like sheep (Howell 1991b). [Pg.742]

Tab. 18.4 Molybdenum content ( Jgkg" dry matter) of liver and kidney from domestic and wild animals, respectively and man... Tab. 18.4 Molybdenum content ( Jgkg" dry matter) of liver and kidney from domestic and wild animals, respectively and man...
A high incidence of renal xanthine calculi and low liver molybdenum concentrations in sheep grazing restricted pastures on the Moutere Hills in New Zealand has been related to their low molybdenum content (0.03 mg Mokg versus 0.4mgkg in healthy pastures Askew 1958). However, xanthine calculi formation was not seen in sheep living on similar low-molybdenum pastures elsewhere, and the suggestion... [Pg.1022]

The Mo-defident kids were in fact born with molybdenum depletion, with their liver containing only 32% of the Mo found in controls. The lack of any age dependency was also striking, as adult Mo-deficient goats were found to have similar Mo contents as 1-day-old kids (Anke et al. 1984a). [Pg.1024]

Zealand by Cunningham.Several experiments by this worker have shown that increased molybdenum intake either naturally from molybdenum-high pastures or from added molybdate reduces the copper content of bovine livers and blood. Data from one of these experiments are given in Table 4. Cunningham claims further that molybdenum rather than copper is the significant factor in the scouring of cattle on copper-deficient peat lands since this symptom occurs where the pastures are moderately low in copper and moderately high in molybdenum but not where the pastures are deficient in copper but contain normal low amounts of molybdenum. [Pg.447]


See other pages where Molybdenum liver content is mentioned: [Pg.1562]    [Pg.1563]    [Pg.1564]    [Pg.1608]    [Pg.1609]    [Pg.1610]    [Pg.390]    [Pg.2]    [Pg.195]    [Pg.5]    [Pg.97]    [Pg.1012]    [Pg.1013]    [Pg.1016]    [Pg.1309]    [Pg.182]    [Pg.526]    [Pg.527]    [Pg.528]    [Pg.497]    [Pg.160]    [Pg.125]    [Pg.446]   
See also in sourсe #XX -- [ Pg.51 , Pg.52 ]




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Molybdenum content

Molybdenum liver

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