During the prenatal period, several complications affecting the mother and the fetus can occur, with consequences for their wellbeing. Preeclampsia (PE), a multisystem progressive disease caused by placental and maternal endothelial dysfunction, usually happens late in pregnancy and complicates 2–8% of pregnancies globally [1]. Moreover, severe and early-onset PE are associated with significant fetal growth restriction (FGR) [2,3], that refers to the fetus that does not grow to its expected biological potential in utero. FGR affects between 3–9% of pregnancies in developed countries and up to 25% in low-middle income countries [4]. According to fetal programming theory, adverse events occurring during critical points of fetal development may cause effects on the offspring and predispose them to chronic diseases later in life [5]. Therefore, placental insufficiency can lead to long-term neurodevelopmental and metabolic diseases, as well as to significant perinatal mortality, especially among prematurely born neonates [6]. However, not only can the FGR predispose the newborn to chronic diseases throughout its life, but prematurity also affects the normal development and the future health of the newborn [5]. Preterm birth (PTB), defined as any birth before 37 completed weeks of gestation, is estimated to be about 11% worldwide [7], i.e., approximately 15 million children are born preterm every year [8]. Prematurity is related to inflammation and oxidative stress pathways [9], and is associated with increased mortality. Many survivors face a wide range of lifetime disabilities, which have financial and organizational consequences on already stretched health services. The World Health Organization (WHO) estimates that more than three-quarters of premature babies can be saved with feasible, cost-effective care [10]. During pregnancy, there is an increase in oxidative stress resulting from placental development, which, under normal conditions, is attenuated by the physiological antioxidant response. The imbalance between oxidative stress and antioxidant response contributes to poor pregnancy outcomes, increasing the risk of PE, FGR and PTB [11,12,13]. Placental ischemia/hypoxia may contribute to oxidative DNA damage due to the release of reactive ROS into the maternal circulation and can act as an enhancer of FGR. In PE, the redox function is also enhanced compared to normal pregnancies [14]. Unbalanced oxidative stress and ROS-produced collagen damage to amniotic membranes are involved not only in PTB but also in premature preterm rupture of membranes (PPROM) [15]. The fetus has to deal with oxidative stress not only in utero, but also at birth, when the newborn has to face a change from an hypoxic environment to a hyperoxic one, which can lead to cytotoxic damage through the creation of ROS and free radicals [16]. Human breast milk contains agents with antioxidant properties, whose concentrations vary during the different stages of lactation, being higher in colostrum. This could impact the antioxidant status of breast-fed infants [17]. Therefore, the intake of antioxidants in breastfeeding mothers could influence the antioxidant concentrations in breast milk, and therefore in breastfed newborns. However, studies on the subject are scarce and the choice of the best antioxidant and best dose to improve neonatal oxidative stress damage remains unknown to date. Antioxidant supplementation during pregnancy and breastfeeding could be a promising and cost-effective tool for preventing or treating all these adverse outcomes.

Globally, there is an ongoing scientific effort to find solutions to prevent and ameliorate health complications that both mothers and newborns may suffer during the perinatal period. Antioxidant supplementation during pregnancy and breastfeeding could be a promising and cost-effective tool for preventing or treating all these adverse outcomes.

Curcumin is a polyphenolic substance generally recognized as safe (GRAS), which comes from the rhizomes of Curcuma longa (turmeric), and has been shown to have antioxidant and anti-inflammatory properties in humans [24]. In addition, it is emerging as a promising adjuvant in the fight against COVID-19 due to its potential to activate NFE2-related factor-2 (Nrf2) and decrease inflammatory cytokines [25]. The therapeutic effect of curcumin to counteract certain complications during pregnancy, such as PE and FGR, has been tested in vitro studies, showing an increase in angiogenesis and a decrease in oxidative stress through activation of the Nrf2 signaling pathway [26,27].

The administration of different doses of this hydrophobic polyphenol by gavage has also been tested in mouse models of fetal restriction by low-protein (LP) diets. In the study carried out by Qi et al. [32], it was observed that a dose of 400 mg/kg/day generated significantly greater fetal gain compared to doses of 100 mg/kg/day and both doses significantly increased fetal and placental weights compared to the untreated LP group. Regardless of dose, in the placenta curcumin reduced levels of oxidative stress marker malondialdehyde (MDA) and of apoptosis to control group levels (without FGR). In contrast, these levels were significantly higher in the untreated LP group. Remarkably, the highest curcumin concentration also restored the percentage of blood sinusoid area in the placenta to control group levels. However, the bioavailability of the antioxidants was not measured in these animals.

2.2. EGCG