Bio: She is a professor and doctoral supervisor at Guizhou Medical University. She has been selected as an Outstanding Young Leading Talent by the university and recognized as Innovative Talent under the Guizhou Provincial High-Level Talent Program. Her research interests include mechanisms and prevention of developmental toxicity induced by environmental toxicants, particularly in the context of neurodevelopment. She is a principal investigator of three projects funded by the National Natural Science Foundation of China (NSFC) and four projects supported by provincial and ministerial agencies. She has published over 30 papers as first or corresponding author in international journals, including Environmental Science & Technology, Science of the Total Environment, and Environment & Health.

Academic affiliations and professional service include: Member, Neurotoxicology Committee, Chinese Society of Toxicology; Vice Chair, Guizhou Environmental Mutagen Society; Member, Environmental and Developmental Origins of Disease Committee, Chinese Environmental Mutagen Society; Youth Editorial Board Member, Chinese Journal of Endemiology Peer reviewer for Journal of Hazardous Materials, Science of the Total Environment, Ecotoxicology and Environmental Safety.

Abstract: Arsenic (As) exposure during pregnancy poses significant risks to fetal development, with growing evidence suggesting sex-specific susceptibility. However, the molecular mechanisms underlying sexually dimorphic placental responses to As remain poorly understood. Pregnant mice were randomly assigned to the control or As-exposed group, with As exposure starting at gestational day 0.5 (GD 0.5) via drinking water, where the As group received 5 ppm As and the control group was given deionized water. Here, we show that maternal As exposure results in fetal As accumulation and a downward trend in fetal weight, while no significant sex-specific differences. In female mice, As-exposed mice placental trophoblast cells exhibited distinct vacuolization and irregular morphology. Quantitative assessment demonstrated As-induced placental remodeling, characterized by a significant expansion of the spongiotrophoblast (SpT) layer concurrent with labyrinthine (Lab) zone reduction, resulting in an elevated SpT/Lab ratio. These pathological alterations were observed consistently in male placental. RNA-seq analysis revealed distinct gene expression profiles between control and As-exposed groups, Further sex-stratified analysis demonstrated differential responses, with female placentas exhibiting 158 up-regulated and 121 down-regulated genes, while male placentas showed more pronounced alterations (294 up-regulated and 327 down-regulated genes). In female group, enrichment was observed in pathways associated with neuron differentiation, nervous system development, neurogenesis, and neuron fate specification; in male group, pathways such as axonogenesis, neuron projection morphogenesis, and regulation of postsynaptic neurotransmitter receptor activity. These findings reveal that As exposure induces sex-specific placental gene expression changes and structural remodeling. Importantly, As exposure may disrupt the sex-dependent execution of placental "developmental scripts" to alter fetal neurodevelopmental trajectories.