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On the nutritive studies of pantothenic acid by antimetabolites. III. Pantothenic acid deficiency produced by -methyl pantothenic acid in rats



On the nutritive studies of pantothenic acid by antimetabolites. III. Pantothenic acid deficiency produced by -methyl pantothenic acid in rats



Tohoku Jour Agric Res 13(4): 397-406



An experiment was conducted in which adult male rats were put on a pantothenic acid deficient diet and a diet to which was added [omega]-methyl-pantothenic acid, which is an antagonist to pantothenic acid for the possible development of pantothenic acid deficiency syndrome. The results are: The rats on a pantothenic acid deficient diet (deficient group) never developed any clear syndrome of deficiency, but those on [omega]-methyl-pantothenic acid containing diet exhibited apparent syndrome of pantothenic acid deficiency: thinning and turning rusty-red of hair, diarrhea and mad behavior. Whether the external signs of deficiency appeared, the p-aminobenzoic acid (PABA) acetylation capacity deteriorated in both the deficient and the antagonist group. Most of the rats in the antagonist group suffered ulcer-like development in the glandular stomach, which was histologically confirmed. The rats in the deficient group did not suffer such definite development, but their stomach wall was found to be thinner than that of rats in the control group. The decrease of Sudan III-positive substance in the adrenal cortex in the deficiency group was the most remarkable in the zona reticularis, followed by the zona fasciculata; but not so great in the zona glomerulosa. By contrast, in the antagonist group, the decrease in this substance not only covered the zona reticularis and the zona fasciculata, but even extended to the zona glomerulosa, showing a sharp decrease. Some rats in the antagonist group met sudden death, but even in these unfortunate ones no exceptional histological findings were obtained in their glandular stomach and adrenal. The possibility of [omega]-methyl-pantothenic acid causing pantothenic acid deficiency in adult rats and the process of detecting the syndrome are discussed.

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