Nutritional Dermatoses in the Rat

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Abstract
The signs resulting from magnesium deprivation were described in 1931–32 by McCollum and Orent, and Kruse, Orent and McCollum. These investigators produced a symptom-complex comprising vasodilatation, hyperirritability of the nervous system, cardiac arrhythmia, spasticity and tonic-clonic convulsions. The experimental diet included only 1.8 parts per million of magnesium, but was considered otherwise adequate. A yeast extract corresponding to approximately a 13.5% level was incorporated into the ration. Assuming that the yeast was a potent source of the vitamin B complex, the diet was probably adequate in all respects, except that it lacked magnesium and vitamin E. Inasmuch as the signs occurred within 1 to 3 weeks, it is likely that the inclusion of vitamin E would not have affected the signs. In 1938, Greenberg and Tufts studied the influence of several factors on the incidence, time of onset, and duration of the peripheral vasodilatation and hyperirritability in magnesium-deficient rats. They stated that the signs were affected by the level of the vitamin B complex, and criticized the use of the alcoholic extract of yeast employed by Kruse, Orent and McCollum, because it was apparently low in factors of the vitamin B complex. Of the several deficiency syndromes produced by deficiencies of the components of the vitamin B complex, pyridoxine deficiency is the only one likely to be confused with magnesium deficiency, because of the apparent similarity of the involvement of the peripherae and the reported convulsive seizures in pyridoxine deficiency (Chick, El Sadr and Worden, '40). The findings in experiment I demonstrated that: (a) the gross signs and symptoms of magnesium deficiency may be differentiated readily from those of pyridoxine deficiency; and (b) the histologic findings in the two diseases are dissimilar. The findings in experiment II demonstrated that: (a) the level of the vitamin B complex exerted no influence on the onset and/or severity of the cutaneous signs and the convulsive seizures, and (b) magnesium deficiency signs in the skin could be produced simultaneously with the healing of the signs of deficiency of the vitamin B complex. The data in experiment II also showed that the magnesium content of the skin is similar in rats subsisting on diets containing adequate and inadequate vitamin B complex. In acute magnesium deficiency the percentage of magnesium of the skin was found to be only slightly lower than the percentage in normal animals. Likewise, the moisture and ash contents and the level of calcium were not significantly altered. When the chemical findings of the magnesium-deficient, vitamin B complex-deficient rats were compared with those of the magnesium-deficient rats that were adequately supplied with the vitamin B complex, the data showed that there was no appreciable influence of the vitamin B complex on the chemical findings. In experiment III it was demonstrated that vitamin E was unrelated to the signs of magnesium deficiency.