The phospholipids of avian spermatozoa are characterized by high proportions of arachidonic (20:4n-6) and docosatetraenoic (22:4n-6) fatty acids and are therefore sensitive to lipid peroxidation. Alpha-tocopherol and glutathione peroxidase [GSH-Px] are believed to be the primary components of the antioxidant system of the spermatozoa. The present study evaluates the effect of vitamin E and vitamin E plus Se supplementation of the cockerel diet on GSH-Px activity, vitamin E accumulation, and lipid peroxidation in the spermatozoa, testes, and liver. At the beginning of the experiment 75 Rhode Island Red cockerels were divided into five groups, kept in individual cages, and fed a wheat-barley-based ration balanced in all nutrients. Supplements fed to the different groups were as follows: vitamin E, 0, 20, 200, 20, and 200 mg/kg to groups 1-5, respectively, with groups 4 and 5 also receiving 0. 3 mg Se/kg. The vitamin E supplementation produced increased levels of alpha-tocopherol in semen, testes, and liver. The inclusion of the Se into the cock diet had a significant (P < 0.01) stimulating effect on GSH-Px activity in seminal plasma, spermatozoa, testes, and liver. The increased vitamin E concentration in the spermatozoa was associated with a reduction in their susceptibility to lipid peroxidation. Similarly, the increased GSH-Px activity provided enhanced protection against lipid peroxidation.

1. The effect of a range of supplementations of vitamin A to the laying hen on the concentration of vitamins A, E, ascorbic acid and carotenoids in the maternal liver, the egg yolk and the embryonic liver were investigated. 2. Four groups of 25 Rhode Island Red hens were fed on standard layer-breeder diets with concentrations of supplemented vitamin A ranging from 0 to 120 micrograms/g retinol equivalents from 28 weeks of age. After 3 months, the concentration of vitamin A in the maternal liver was found to be greatly enhanced in proportion to the increasing rates of supplementation with the vitamin. However, the concentration of vitamin E in the maternal liver was markedly reduced by high dietary contents of vitamin A. 3. The concentration of vitamin A in the yolk of the hens' eggs was markedly increased by the dietary supplementation. However, the concentration of both vitamin E and carotenoids in the yolks were significantly reduced by high dietary contents of vitamin A. 4. The concentration of vitamin A in the liver of the embryo and the day old chick was greatly increased by the high concentrations of maternal vitamin A provision. However, the concentration of vitamin E, carotenoids and ascorbic acid in the embryonic/neonatal liver were significantly reduced by high contents of vitamin A in the maternal diet. 5. The susceptibility of the embryonic/neonatal liver to lipid peroxidation was significantly increased as a result of high provisions of maternal vitamin A. 6. It is concluded that 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.

The relationship between the levels of the lipid‐soluble antioxidants, α‐tocopherol and carotenoids, in the parental diet, the yolk and the neonatal tissues was investigated for four avian species of commercial importance. The chicken displayed a much greater efficiency in incorporating α‐tocopherol from the parental diet into the yolk in comparison with the turkey, duck and goose. Thus, in spite of similar concentrations in the respective diets, the resultant concentration of α‐tocopherol in the yolk of the chicken egg was four to five times greater than observed for the other three species. A similar but less dramatic picture was observed for carotenoids: identical dietary provision of carotenoids in the maternal feeds resulted in the chicken eggs displaying between 1·4 and 1·9 times the concentration in the yolk than was observed for the other three species. These differences between the species regarding the levels of α‐tocopherol and carotenoids in the yolk were closely reflected in the subsequent concentrations of these components in the livers of the hatchlings. Thus, the concentrations of α‐tocopherol and carotenoids in the liver of the day‐old chicken were respectively about three and two times greater than in the livers of the other three species. Although the water‐soluble antioxidant, ascorbic acid, is synthesised by the embryo as opposed to provision via the maternal diet and the yolk, the concentration of this component in the brain of the day‐old chicken was approximately 50% greater than in the brains of the other three species. Thus, it is possible that the antioxidant capacity of the developing turkey, duck and goose may be compromised under conditions of commercial production. All four species displayed a rapid depletion of α‐tocopherol and carotenoids from the livers during the first 9 days after hatching. © 1998 SCI.

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1. The effect of increasing vitamin A doses on the concentrations of vitamins A, E, ascorbic acid and carotenoids in the liver and blood plasma of the neonatal chick were investigated. 2. In the 1st experiment 75 d-old chickens were divided into 3 equal groups and in the 2nd experiment 100 d-old chickens were divided into 5 groups. Retinyl acetate in corn oil (1.72; 4.30; 8.60 or 17.2 mg) was intubated directly into the crop daily during the first 5 d after hatch. 3. The intubation of vitamin A increased its accumulation in the liver, with a plateau at about 6,000 microg/g, and was associated with inhibition of vitamin E and carotenoid utilisation from the liver during postnatal development. 4. Moderate amounts of vitamin A intubation increased ascorbic acid concentration in the liver, kidney, brain and plasma. A further increase in vitamin A intubation had an adverse effect on ascorbic acid concentrations in the plasma and brain. 5. The 2 highest inputs of vitamin A decreased glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities in the chicken liver and brain. 6. It is concluded that the effect of vitamin A on development of the antioxidant system in the neonatal chick is dose-dependent and an excess of vitamin A can compromise the antioxidant defence system.