The clinical signs of vitamin A toxicity in poultry include weight loss; decreased feed intake; swelling and crusting of the eyelids to the extent that they become sealed closed; inflammation of the mouth, nares, adjacent skin and skin of the feet; decreased bone strength; bone abnormalities; and mortality (Scott et al., 1982). Skin lesions at the commissure of the beak, nose and eyes attributable to mucous membrane hyperplastic activity have been shown to occur in chicks within 72 hours after oral dosing with 60,000 IU vitamin A (Kriz and Holman, 1969). Excessive provision of vitamin A to the laying hen results in an adverse effect on vitamin E, carotenoids and ascorbic acid in the embryonic/neonatal liver and can compromise the antioxidant status of the progeny (Surai et al., 1998).
It is believed that release of lysosomal enzymes is responsible for degradative changes observed in tissues and intact animals suffering from hypervitaminosis A (Fell and Thomas, 1960). In hypervitaminosis A, retinol penetrates the lipid of the membrane and causes it to expand, and because the protein of the membrane is relatively inelastic, the membrane is weakened. Thus, many phenomena in hypervitaminosis can be explained in terms of damage to membranes either in cells or of organelles within cells.
Excess vitamin A affects metabolism of other fat-soluble vitamins via competition for absorption and transport. Therefore, in diets containing barely adequate levels of vitamins D, E and K, a marked increase in dietary vitamin A may cause decreases in growth or egg production due to a deficiency of one or more of the other fat-soluble vitamins rather than a toxic effect of vitamin A. Retinoid-induced hemorrhaging in rats fed diets deficient in vitamin K has been reported (McCarthy et al., 1989). The mechanisms of absorption and transport are similar for the carotenoid pigments and the fat-soluble vitamins. A marked increase in dietary vitamin A has been shown to interfere with absorption of carotenoids, thereby resulting in decreased pigmentation for poultry. While the absolute level of vitamin A supplementation is important, the ratio of vitamin A to the other fat-soluble vitamins is likewise of significance.
High dietary levels of vitamin A impede the utilization of vitamin D3 in broilers fed low levels (500 IU per kg or 227 IU per lb) of supplemental vitamin D3 (Aburto and Britton, 1998b). In the presence of low levels of vitamin D, the addition of vitamin A reduced body weight and bone ash and resulted in rickets. It is not uncommon to encounter field rickets when these levels of vitamin A are fed, even though the level of vitamin D would normally be considered more than adequate.
Route of administration of vitamin A has an influence on the toxicity of the vitamin. In chicks and poults, levels of vitamin A that caused adverse changes in body weight, packed cell volume, serum calcium or phosphorus, or bone ash were 100 times the NRC requirement when birds were fed ad libitum, but only 10 times the NRC level when birds were fed via gavage.
