Maternal exposure to a mixture of di(2-ethylhexyl) phthalate (DEHP) and polychlorinated biphenyls (PCBs) causes reproductive dysfunction in adult male mouse offspring. | LitMetric
We investigated the effects of maternal exposure to the plasticizer di(2-ethylhexyl) phthalate (DEHP) and the organic industrial compounds polychlorinated biphenyls (PCBs), singly and combined, on the reproductive function of male mouse offspring. Mice dams were exposed throughout pregnancy and lactation to 1μg PCBs (101+118)/kg/day, 50μg DEHP/kg/day, or the DEHP/PCB mixture in the diet. The mixture induced permanent alterations in adult F1 males' reproductive health in a way, differently from the single compounds. Depending on the endpoint, we observed: (1) synergy in altering the gross and histological morphology of the testis; (2) antagonism on the expression levels of genes involved in pituitary-gonadal cross-talk; (3) non-interactions on sperm parameters and testosterone production. This study illustrates the complex action of a DEHP/PCB mixture, leading to a unique panel of effects on the male reproductive system, indicating the need for research on the reproductive hazards of combined endocrine disruptors.
Environmental exposures, including air pollutants and lack of natural spaces, are associated with suboptimal health outcomes in children. We aimed to study the associations between environmental exposures and gene expression in children. Associations of exposure to particulate matter (PM) with diameter <2.
Background: Youth is a period with exposure to high risk of reproductive health (RH) problems. Despite, several strategies designed to solve these problems, youths are experiencing unsafe abortion, unintended pregnancy, and sexually transmitted infections (STIs) so far. The utilization of Youth Friendly Services (YFS) and its determinants has not been well studied in Gambella so far.
Industrialization has led to significant increases in the types and quantities of pollutants, with environmental pollutants widely present in various media, including the air, food, and everyday items. These pollutants can enter the human body via multiple pathways, including ingestion through food and absorption through the skin; this intrusion can disrupt the production, release, and circulation of hormones in the body, resulting in a range of illnesses that affect the reproductive, endocrine, and nervous systems. Consequently, these pollutants pose substantial risks to human health.
This study investigated the impact of maternal high-fat diet on vascular function and endothelial homeostasis in offspring. We found that offspring exposed to maternal high-fat diet exhibited elevated blood pressure, impaired abdominal aortic vascular function, and endothelial homeostasis imbalance. These changes were accompanied by increased levels of reactive oxygen species (ROS) and upregulation of pro-inflammatory cytokines (including IL-1β, TNF-α, IL-6, and IL-10).
Introduction: Pregnant individuals who smoke face increased health risks because smoking harms both the mother and their developing offspring.
Methods: Using 307 417 Europeans from the UK Biobank, we examined whether exposure to maternal smoking during pregnancy (MSP) interacts with genetic risk to predict offspring birth weight (BW) and smoking behaviors. We investigated interactions between MSP and genetic risk at multiple levels: single variant, gene-level, and polygenic score.
