Decabromodiphenyl Ethane (DBDPE), a kind of new brominated flame retardants (NBFRs) used to replace DecaBDE, has been frequently detected in the environment and human samples. In this study, we explored its toxic effects on male mouse offspring after perinatal exposure to DBDPE. During the perinatal period, pregnant ICR mice were exposed to DBDPE (100 μg/kg body weight) via oral gavage. After weaning, male offspring were fed on a low-fat diet and a high-fat diet, respectively. We measured and recorded body weight, liver weight, and epididymis fat mass, blood biochemical markers, metabolites changes in liver, and gene expression involved in lipid and glucose homeostasis. The results showed that perinatal exposure to DBDPE increased the risk of obesity in mouse offspring and affected triglyceride synthesis, bile secretion, purine synthesis, mitochondrial function and glucose metabolism, furthermore, the use of HFD feeding may further exacerbate these effects. All of these results show that early-life exposure to low doses of DBDPE can promote the development of metabolic dysfunction, which in turn induces obesity.

Xenobiotics are worldwide distributed and humans are unavoidably exposed to multiple chemical compounds during life, from preconception to adulthood. The human microbiota is mainly settled during early life and modulate host health and fitness. One of the main routes for chemical exposure is by intake of contaminated food and water. Thus, the interplay between diet-xenobiotics-microbiota during pregnancy and perinatal period may have relevant consequences for infant and adult health. Maternal exposure to metal(oid)s, persistent organic pollutants, and some food additives can modify the infant’s microbiota with unknown consequences for child or adult health. Toxicants’ exposure may also modulate the maternal transfer of microorganisms to the progeny during birth and breastfeeding; however, scarce information is available. The rapid increase in releasing novel chemicals to the environment, the exposure to chemical mixtures, the chronic/low dose scenario, and the delay in science-stakeholders action call for novel and groundbreaking approaches to improve a comprehensive risk assessment in sensitive population groups like pregnant women and neonates, with emphasis on microbiota as modulating factor and target-organ of xenobiotic’s toxicity.

Deca-bromodiphenyl ether (BDE-209) regulates various aspects of spermatogenesis and male fertility through its effect on estrogen receptor α (ERα), but the underlying mechanism remains unclear. Because molecular mechanisms such as remodeling of the blood-testis barrier (BTB) play crucial roles in spermatogenesis, we investigated the disruptive effects of ERα agonists on the BTB in spermatogenesis. In this study, 0, 300, and 500 mg/kg/day of BDE-209 were administered to pregnant adult mice by oral gavage from gestation day 7 to postnatal day 21. SerW3 cells were treated with methylpiperidino pyrazole (MPP) for 30 min before being treated with 50 μg/mL of BDE-209. BDE-209 increases ERα in time- and dose-dependent manners and decreases formin 1 and BTB-associated protein in F1 male mice. Furthermore, BDE-209 impairs the structure and function of the BTB. Activation of ERα signaling could disrupt the BTB, leading to spermatogenesis dysfunction. The results identified the role of ERα in BTB disruption during spermatogenesis and suggested that BTB disruption occurs because of exposure to BDE-209, which could potentially affect spermatogenesis. In conclusion, Sertoli cells seem to be the primary target of BDE-209 in the perinatal period, and this period constitutes a critical window of susceptibility to BDE-209. Also, the SerW3 cell model may not be a particularly useful cell model for studying the function of the cytoskeleton.

The present study evaluated the protective effects of Centella asiatica (CA) leaf extract on behavioral deficits and neurotoxicity in adult rat exposed to lead during perinatal period. Adult Wistar rats were exposed to 0.15% lead acetate (Pb) from gestation day 6 through drinking water and the pups were exposed lactationally to Pb till weaning. Significant perturbations in locomotor activity and exploratory behavior were observed in rats exposed to Pb during perinatal period. The levels of lipid peroxidation increased significantly with a reduction in levels of glutathione and activity levels of acetylcholinesterase and antioxidant enzymes in hippocampus, cerebrum, cerebellum, and medulla of brains excised from Pb-exposed rats. Oral supplementation of CA during postweaning period provided significant protection against Pb-induced behavioral impairments and neurotoxicity, without chelating tissue Pb levels. The possible neuroprotective efficacy of CA may be due to its antioxidant potential but not by lowering effects of brain Pb content.