Prenatal independent and combined effects of yolk vitamin E and corticosterone on embryo growth and oxidative status in the yellow-legged gull

Abstract

Variation in the concentration of antioxidants and hormones of maternal origin in the eggs of birds can have profound influences on offspring phenotype both pre- and post-natally. Egg maternal substances, however, can have interacting effects, but experimental studies of the consequences of the combined variation in the egg concentration of such molecules are extremely rare, particularly as far as prenatal stages are considered. We manipulated the yolk concentrations of vitamin E and corticosterone, which are the main antioxidants and, respectively, the main glucocorticoid hormone in bird eggs, both independently and simultaneously and we tested their separate and combined effects on growth and oxidative status in the liver and in the brain of yellow-legged gull (Larus michahellis) embryos. Egg supplementation of relatively large, yet physiological doses of corticosterone depressed embryo growth (total body mass, tarsus length and liver mass) while administration of vitamin E in association with corticosterone restored normal growth. Vitamin E did not affect embryo growth when administered alone. We further analyzed independent and combined effects of vitamin E and corticosterone on liver and brain total antioxidant capacity, concentration of reactive oxygen molecules and lipid peroxidation. Vitamin E significantly reduced liver total antioxidant capacity, while corticosterone depressed brain lipid peroxidation. Prenatal exposure to vitamin E and corticosterone appears to have antagonistic effects on body growth, although vitamin E is not limiting in yellow-legged gull eggs. In combination with the results of previous experiments on the same species applying smaller experimental doses or focusing on the post-natal rather than pre-natal life stages, our findings indicate that the effects of a physiological increase in the egg concentrations of these substances can be life stage- and dose-specific, implying that generalizing prenatal effects of egg compounds may not be feasible.