ABSTRACT: 1. The metabolism of 5,6-monoepoxyvitamin A aldehyde in the rat was found to be identical with that of vitamin A aldehyde. It promptly alleviated all the symptoms of vitamin A deficiency and promoted the growth of the vitamin A-deficient rats. 2. When administered orally, 5,6-monoepoxyvitamin A aldehyde was reduced to the corresponding alcohol in the intestine and esterified before being transported to the liver for storage. 3. 5,6-Monoepoxyvitamin A aldehyde was not converted into the furanoid form, 5,8-monoepoxyvitamin A aldehyde, during passage through the stomach. 4. Intraperitoneal administration of 5,6-monoepoxyvitamin A aldehyde led to the accumulation of 5,6-monoepoxyvitamin A in the liver and other tissues. Subcutaneous administration of this compound alleviated all the symptoms of vitamin A deficiency. 5. The small intestine is the major, if not the only, site for the metabolic reduction of 5,6-monoepoxyvitamin A aldehyde and its subsequent esterification. 6. It was demonstrated that the rat possesses the necessary enzymes for the reduction and oxidation of 5,6-monoepoxyvitamin A aldehyde to the corresponding alcohol and acid as well as the esterification of 5,6-monoepoxyvitamin A alcohol to its palmitate. These metabolic conversions were shown to be as efficient as those of vitamin A aldehyde and alcohol. 7. 5,6-Monoepoxyvitamin A aldehyde possesses a biological potency 108% that of all-trans vitamin A acetate. 8. A new visual pigment with lambda(max.) 480mmu, along with natural rhodopsin, was isolated from the retinas of rats maintained on 5,6-monoepoxyvitamin A aldehyde. 9. Oral administration of 5,8-monoepoxyvitamin A aldehyde to vitamin A-deficient rats led to the accumulation of 5,8-monoepoxyvitamin A in the liver and other tissues. Enzymic reduction and oxidation of 5,8-monoepoxyvitamin A aldehyde to its alcohol and acid, as well as the esterification of the alcohol, were demonstrated.
