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 a profound influence on offspring phenotype both prenatally and postnatally. Egg maternal substances 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 concerned. We manipulated the yolk concentration of vitamin E and corticosterone, which are, respectively, the main antioxidant and 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 physiological doses of corticosterone depressed embryo growth (total body mass, tarsus length and liver mass), whereas administration of vitamin E in association with corticosterone restored normal growth. Vitamin E did not affect embryo growth when administered alone. We further analysed the independent and combined effects of vitamin E and corticosterone on liver and brain total antioxidant capacity, the 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 postnatal rather than prenatal life stages, our findings indicate that the effects of a physiological increase in the egg concentration of these substances can be life stage and dose specific, implying that generalizing prenatal effects of egg compounds may not be feasible.