Prevention of Allylisopropylacetamide Induced Experimental Porphyria in the Rat by Vitamin E

Abstract

VITAMIN E deficiency in experimental animals is characterized by species specific manifestations affecting a variety of tissues and organs such as the muscle, the gonads and the brain^1–3. In man and in primates, recent studies have shown the existence of an anaemia associated with a lack of this vitamin; the locus of the metabolic defect is believed to reside in the biogenetic sequence leading to porphyrins and haem^4–7. We have recently shown the existence of a similar metabolic defect in haem synthesis in the bone marrow of vitamin E deficient rats, which suggests a mechanism of action common to all animal species (H. S. M., Pinelli and P. P. N., unpublished results). Although no unifying concept has been proposed to explain the apparent pleomorphism in the syndromes of vitamin E deficiency, it has been suggested that “trace lipids” such as fat soluble vitamins could function as regulators of vital metabolic processes at the molecular level⁸.