Embryonic exposure to corticosterone modifies the juvenile stress response, oxidative stress and telomere length

Abstract

Early embryonic exposure to maternal glucocorticoids can broadly impact physiology and behaviour across phylogenetically diverse taxa. The transfer of maternal glucocorticoids to offspring may be an inevitable cost associated with poor environmental conditions, or serve as a maternal effect that alters offspring phenotype in preparation for a stressful environment. Regardless, maternal glucocorticoids are likely to have both costs and benefits that are paid and collected over different developmental time periods. We manipulated yolk corticosterone (cort) in domestic chickens (Gallus domesticus) to examine the potential impacts of embryonic exposure to maternal stress on the juvenile stress response and cellular ageing. Here, we report that juveniles exposed to experimentally increased cort in ovo had a protracted decline in cort during the recovery phase of the stress response. All birds, regardless of treatment group, shifted to oxidative stress during an acute stress response. In addition, embryonic exposure to cort resulted in higher levels of reactive oxygen metabolites and an over-representation of short telomeres compared with the control birds. In many species, individuals with higher levels of oxidative stress and shorter telomeres have the poorest survival prospects. Given this, long-term costs of glucocorticoid-induced phenotypes may include accelerated ageing and increased mortality.

Figure 1.

The effect of elevated embryonic corticosterone on plasma corticosterone concentration (mean ± s.e.m.) during an acute stress response in juvenile chickens (all groups, n = 7). Filled circles with solid line, control; squares with solid line, low cort; filled diamonds with solid line, high cort.

Figure 2.

Relationships between reactive oxygen metabolites (ROMs) and total antioxidant capacity (TAC) within treatment groups at the initiation (INITIAL) and after (POST) an acute stressor. Least square mean ± s.e.m. plotted (all groups, n = 7). Filled circles, control; squares, low cort; diamonds, high cort.

Figure 3.

The effect of elevated embryonic corticosterone on telomere restriction fragment (TRF) length of juvenile chickens measured at 21 days of age. Plotted are mean (± s.e.m.) TRF frequency distributions from chicken erythrocytes against molecular weight (MW). The data are log transformed and then fit by least-squares fourth-order polynomial regression using the equation: log(freq) = ß₀ + ß₁ (MW) + ß₂ (MW − medianMW)² + ß₃ (MW − medianMW)³ + ß₄ (MW − medianMW)⁴. Analysis was performed on the 12 TRF intervals denoted by the arrows (see text; all groups n = 7). Filled circles with solid, control; squares with solid line, low cort; diamonds with solid line, high cort.