Lactation attenuates pro-oxidant reactions in the maternal brain

Reactive oxygen species (ROS) are intimately linked to bioenergetics and redox biology, contributing to cellular functioning and physiological signaling, but also acting as toxic agents during oxidative stress. Hence, the balance between pro-oxidant reactions and the activity of antioxidant defenses sustains a basal oxidative status, controls the increase of redox signaling, and mediates potential pathological events during oxidative stress. Maternal experience, especially during nursing, requires high energetic demands and expenditure to ensure the well-being of the offspring. The mother must adapt from satisfying her own needs to additionally fulfilling those of her descendants. Oxidative stress has been proposed as one of the reproductive trade-off hallmarks. However, the oxidative shielding hypothesis has also been proposed in the context of reproduction. The reproductive experience induces a wide range of well-documented changes in the female brain, which potentially lead to protection against the enhanced oxidative activity. To date, the metabolic and cellular mechanisms that underlie lactation-induced neuroprotection against oxidants are unknown. The neuroendocrine changes in the brain of the lactating dam promote diminished propensity to excitotoxic brain injury and stress, as well as enhanced neuroprotection and plasticity. In addition to review studies on the oxidant balance due to motherhood, we included new data from our laboratory, addressing the importance of measuring pro-oxidant reactions in separated brain regions. The hippocampus of lactating rats exhibits lower levels of pro-oxidant reactions than that of virgin rats, supporting the oxidative shielding hypothesis in lactation.