The persistent effects of stress during lactation on maternal and offspring mitochondria

Abstract

An increase of circulating glucocorticoids in reproductive females may augment allocation of resources towards self-maintenance and away from offspring. Thus, elevated circulating glucocorticoids may negatively affect offspring development. However, maternal stress may induce preparative responses in offspring, such as higher tolerance to oxidative stress and more efficient mitochondria, which could positively impact survival. To test this hypothesis, corticosterone (CORT) was administered orally to female mice from days 7 to 21 after parturition. Thus, offspring were indirectly exposed to CORT through the mother’s milk and aspects of their mitochondrial physiology were investigated at two timepoints, 5.5 weeks and 10 weeks of age. At both ages, mitochondria were isolated from liver and skeletal muscle to measure respiratory control ratio (RCR) and reactive oxygen species (ROS) production. Oxidative damage markers of protein oxidation and lipid peroxidation were quantified in each tissue. While effects on maternal mitochondrial physiology were limited, there were numerous effects of maternal stress on offspring. These include beneficial effects on mitochondrial respiration and lower ROS production in skeletal muscle tissue, as well as reduced oxidative damage markers in both tissues. Many of these effects were only revealed or often strengthened with offspring aging.