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(1962a,b) concluded that the magnesium requirement of weanling Beagle pups fed a purified diet was 140 mg/kg, while the requirement for mature dogs ranged from 80 to 180 mg/kg. They also reported that the severity of the magnesium deficiency syndrome was increased by elevation of the dietary calcium and phosphorus concentrations from 0.6 to 0.9 percent and 0.4 to 0.9 percent, respectively. Vitale et al. (1961) fed magnesium-deficient diets to dogs and observed a series of changes that did not occur in dogs fed the basal diet with 960 mg magnesium and 5,000 mg potassium added per kilogram diet. This high magnesium concentration was presumably used to ensure an adequate intake. Kahil et al. (1966) reported dogs fed diets containing 5 mg magnesium per kilogram developed convulsive seizures and alterations in sodium and potassium transport, whereas dogs receiving 16 mg magnesium as anhydrous magnesium oxide per kilogram of body weight per day did not have any clinical signs of deficiency. Morris (1963) reported that when weanling puppies were fed diets containing 30, 100, or 320 mg magnesium per kilogram, the calcium concentrations in the aorta were 8,320; 5,450; and 980 mg/kg (dry tissue), respectively, indicating an interaction in the absorption or retention of these minerals. Romsos et al. (1976) used magnesium oxide concentrations ranging from 0.025 to 0.035 percent (250 to 350 mg/kg) in experimental purified diets without observing any clinical signs of magnesium deficiency. Based on the foregoing data, the magnesium requirements for dogs should be met by dietary concentrations of 0.11 g/1,000 kcal ME.

Signs of Deficiency

Anorexia, vomiting, decreased weight gain, and hyperextension of the front legs were observed in puppies (7 to 9 weeks of age initially) that were fed a purified diet containing less than 5 mg/kg magnesium for 3 weeks (Kahil et al., 1966). By 4 to 6 weeks the puppies fed this diet showed irritability, ataxia of hind legs, convulsive seizures, and alterations in sodium and potassium transport. Similar deficiency signs were reported in puppies fed a magnesium-deficient diet containing 0.6 percent calcium and 0.5 percent phosphorus with 8 percent fat (Bunce et al., 1962a). These authors reported that the dogs' blood serum magnesium and calcium concentrations were depressed and that their inorganic phosphorus was elevated. At necropsy, aortas of these animals contained extreme mineralized lesions, primarily calcium and phosphorus deposits. They also reported that a much longer depletion period was required to demonstrate magnesium deficiency in mature dogs than in puppies. In mature dogs there was a loss in body weight and a depression in serum magnesium but no changes in serum calcium or phosphorus. Vitale et al. (1961) recorded electrocardiographic changes in puppies fed magnesium-deficient diets that were similar to those seen in hyperkalemia. Subsequent studies in 4- to 6-month-old dogs demonstrated a relationship between magnesium and potassium deficiencies. Hyperkalemia and marked electrocardiographic changes were recorded in two dogs that received a low magnesium diet for 9 months; these changes were similar to those observed in dogs deficient in both magnesium and potassium.


Both iron and copper are essential for preventing anemia. Most of the iron is in the respiratory pigments (hemoglobin and myoglobin) and in various enzymes. The characteristic anemia associated with an iron deficiency is of a hypochromic, microcytic type. However, hypochromic anemias may also occur when the total iron content of the body is normal, indicating that factors other than total body iron are also involved (Moore, 1963). Usually, 5 to 10 percent of the oral iron intake is absorbed (Stewart and Gambino, 1961; Talwar et al., 1961; Pollack et al., 1963, 1964). However, many factors influence absorption, including the chemical form of the iron (Brown, 1963; Fritz et al., 1970), associated food proteins (Fitch et al., 1964), mineral balance of the diet, hormone balance (Cline and Berlin, 1963), freedom from intestinal abscesses (Hahn et al., 1946), vitamin stores, severity of anemia (Koepke and Stewart, 1964a,b), and diurnal variations (Goldstone et al., 1962). The gastric juice from anemic dogs contains a substance that increases the absorption of iron from the gastrointestinal tract. When the gastric juices from anemic dogs and iron were given to normal dogs, the absorption of iron was significantly increased (Koepke and Stewart, 1964a,b; Arriaga de la Cabada et al., 1969).

The iron of wheat bran has been shown to be as available for dogs as that of ferric pyrophosphate, but that of spinach is less than half as available (Frost et al., 1940). These findings conform with the relative availability of the iron in those three sources when fed to rats and suggest that availability for the rat may be used as a guide for dogs. Elvehjem et al. (1933, 1934) and Sherman et al. (1934) have shown the iron of inorganic salts, liver, heart, muscle, and soybeans to be readily available (50 percent or more utilized), while the utilization from oysters, alfalfa, spinach, blood, wheat, oats, and yeast was lower (25 percent utilized). Dogs utilize iron from porphyrin compounds, such as hemoglobin and myoglobin (Udall and McCay, 1953; Bannerman, 1965). There are variations in the efficiency with which various species utilize iron from iron-containing salts. Ferric ammonium

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