Maternal Disononyl Phthalate Exposure Activates Allergic Airway Inflammation via Stimulating the Phosphoinositide 3-kinase/Akt Pathway in Rat Pups

Objective To evaluate the effect of diisononyl phthalate（DINP） exposure during gestation and lactation on allergic response in pups and to explore the role of phosphoinositide 3-kinase/Akt pathway on it. Methods Female Wistar rats were treated with DINP at different dosages（0, 5, 50, and 500 mg/kg of body weight per day）. The pups were sensitized and challenged by ovalbumin（OVA）. The airway response was assessed; the airway histological studies were performed by hematoxylin and eosin（HE） staining; and the relative cytokines in phosphoinositide 3-kinase（PI3K）/Akt pathway were measured by enzyme-linked immunosorbent assay（ELISA） and western blot analysis. Results There was no significant difference in DINP＇s effect on airway hyperresponsiveness（AHR） between male pups and female pups. In the 50 mg/（kg·d） DINP-treated group, airway response to OVA significantly increased and pups showed dramatically enhanced pulmonary resistance（RI） compared with those from controls（P〈0.05）. Enhanced Akt phosphorylation and NF-κB translocation, and Th2 cytokines expression were observed in pups of 50 mg/（kg·d） DINP-treated group. However, in the 5 and 500 mg/（kg·d） DINP-treated pups, no significant effects were observed. Conclusion There was an adjuvant effect of DINP on allergic airway inflammation in pups. Maternal DINP exposure could promote OVA-induced allergic airway response in pups in part by upregulation of PI3K/Akt pathway.

Maternal Lead Exposure Induces Down-regulation of Hippocampal Insulin-degrading Enzyme and Nerve Growth Factor Expression in Mouse Pups

Lead exposure is a known potential risk factor for neurodegenerative diseases such as Alzheimer’s disease （AD）. Exposure to lead during the critical phase of brain development has been linked with mental retardation and hypophrenia in later life.

Maternal Bisphenol B Exposure and Mammary Gland Development of Offspring:A Time-Series Analysis

Breast cancer incidence has increased and become the world’s most prevalent cancer,which is related to abnormal development of mammary glands and thought to be influenced by environment endocrine disruptors such as bisphenol A(BPA).However,whether its substitution,bisphenol B(BPB),has similar effects remains a concern.In the present study,a maternal exposure model of ICR mice combined time-series RNA-seq analysis was established to explore the underlying correlation among maternal BPB exposure(300μg/kg body weight),mammary gland development,and long-term breast health in offspring.The results showed that BPB exposure disrupted hormonal homeostasis of the female offspring but did not affect the branch development of mammary glands in a time-dependent manner.However,at postnatal day 90(PND90),BPB exposure resulted in duct dilatation,lobular hyperplasia,and inflammatory cell infiltration and increased the number of hormone receptor-expressing(HR+)luminal cells in offspring.Further,the differentially expressed genes in time-series analysis of RNA-seq for mammary glands of the female offspring were enriched in the morphogenesis of branching structures,branching epithelium,and branching morphogenesis of epithelial tubes,which are always considered gland development.Interestingly,the results of RNA-seq also suggested that progesterone receptor(Pgr)mRNA expression in the BPB group was elevated at PND90,and breast cancer related genes such as GATA binding protein 3(Gata3)and epidermal growth factor receptor(Egfr)were also altered.These findings suggested that maternal BPB exposure did not accelerate mammary gland development or lead to obvious morphological anomalies of offspring,but it induced pathological changes and altered cancer related gene expression in adult offspring breast.

Risk factors for hypospadias in China

This case-controlled study was designed to evaluate the association between various baseline parental factors and the risk of hypospadias in China. Patients were selected from tertiary referral hospitals in Anhui, a province in mid-eastern China. A questionnaire was given to the parents of each patient. The final database included 193 cases and 835 controls. The incidence of additional coexistent anomalies was 13.0%, primarily cryptorchidism （9.8%）. Ten patients （5.1%） were from families with genital anomaly, including five families （2.6%） with hypospadias. The risks of hypospadias was higher for children of mothers 〉 35 （odds ratio [OR] =1.47） and 〈 18 （OR = 2.95） years of age, and in mothers who had consumed alcohol （OR = 2.67）, used drugs （OR = 1.53） and had an infection （OR = 1.87） during pregnancy. The risk of hypospadias was also higher when mothers （OR = 1.68） and fathers （OR = 1.74） were engaged in agriculture. Other factors assessed were not associated with the risk of hypospadias.

Developmental impacts and toxicological hallmarks of silver nanoparticles across diverse biological models

Silver nanoparticles(AgNPs),revered for their antimicrobial prowess,have become ubiquitous in a range of products,from biomedical equipment to food packaging.However,amidst their rising popularity,concerns loom over their possible detrimental effects on fetal development and subsequent adult life.This review delves into the developmental toxicity of AgNPs across diverse models,from aquatic species like zebrafish and catfish to mammalian rodents and in vitro embryonic stem cells.Our focus encompasses the fate of AgNPs in different contexts,elucidating associated hazardous results such as embryotoxicity and adverse pregnancy outcomes.Furthermore,we scrutinize the enduring adverse impacts on offspring,spanning impaired neurobehavior function,reproductive disorders,cardiopulmonary lesions,and hepatotoxicity.Key hallmarks of developmental harm are identified,encompassing redox imbalances,inflammatory cascades,DNA damage,and mitochondrial stress.Notably,we explore potential explanations,linking immunoregulatory dysfunction and disrupted epigenetic modifications to AgNPsinduced developmental failures.Despite substantial progress,our understanding of the developmental risks posed by AgNPs remains incomplete,underscoring the urgency of further research in this critical area.