Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2026
Study on the effects of gestational arsenic exposure on the developmental toxicity of brain tissue in mice offspring using network toxicology and RNA-seq.
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Wang Zitong, Qiao Wenjin, Liu Ruigang, Lv Yuan, Niu Binjie, Li Tianxu, Zhang Mengling, Xiang Yanhui, Qiao Rui, Tai Dapeng
Аннотация
BACKGROUND: Long-term arsenic exposure is associated with health risks, including neurotoxicity, cardiovascular diseases, and cancer, with heightened vulnerability during early development. This study integrates RNA sequencing (RNA-seq) and network toxicology to construct a competing endogenous RNA (ceRNA) network and elucidate molecular mechanisms of prenatal arsenic-induced neurodevelopmental toxicity.
METHODS: Pregnant ICR mice were exposed to sodium arsenite (NaAsO2, 0.5 ppm) through drinking water. Behavioral tests were performed on postnatal day 30 (PND 30). A total of 20 offspring mice (male/female = 1:1) underwent behavioral assessments, including open field, forced swim, and tail suspension tests, to evaluate anxiety- and depression-like behaviors. Neonatal brain tissues were collected on postnatal day 1 (PND 1) and analyzed using RNA sequencing. The results were further integrated with network toxicology analyses and were subsequently validated experimentally.
RESULTS: Prenatal arsenic exposure elicited significant anxiety- and depression-like behaviors in offspring. Integrated analyses showed that disrupted ceRNA regulatory axes converge the calcium-signaling pathway, neuroactive ligand-receptor interaction, and synaptic-vesicle cycle, revealing key molecular mechanisms underlying the observed neurodevelopmental impairments.
CONCLUSION: This study demonstrates that prenatal arsenic exposure induces early molecular perturbations in the neonatal brain by altering competing endogenous RNA regulatory networks. More importantly, the integration of transcriptomic data with network-based analyses provides a systematic framework for elucidating the underlying mechanisms of developmental neurotoxicity, highlighting key signaling pathways associated with synaptic function and neuronal communication. This network-oriented approach offers mechanistic insights beyond single-gene analysis and facilitates the identification of critical regulatory processes involved in arsenic-induced neurodevelopmental effects.
METHODS: Pregnant ICR mice were exposed to sodium arsenite (NaAsO2, 0.5 ppm) through drinking water. Behavioral tests were performed on postnatal day 30 (PND 30). A total of 20 offspring mice (male/female = 1:1) underwent behavioral assessments, including open field, forced swim, and tail suspension tests, to evaluate anxiety- and depression-like behaviors. Neonatal brain tissues were collected on postnatal day 1 (PND 1) and analyzed using RNA sequencing. The results were further integrated with network toxicology analyses and were subsequently validated experimentally.
RESULTS: Prenatal arsenic exposure elicited significant anxiety- and depression-like behaviors in offspring. Integrated analyses showed that disrupted ceRNA regulatory axes converge the calcium-signaling pathway, neuroactive ligand-receptor interaction, and synaptic-vesicle cycle, revealing key molecular mechanisms underlying the observed neurodevelopmental impairments.
CONCLUSION: This study demonstrates that prenatal arsenic exposure induces early molecular perturbations in the neonatal brain by altering competing endogenous RNA regulatory networks. More importantly, the integration of transcriptomic data with network-based analyses provides a systematic framework for elucidating the underlying mechanisms of developmental neurotoxicity, highlighting key signaling pathways associated with synaptic function and neuronal communication. This network-oriented approach offers mechanistic insights beyond single-gene analysis and facilitates the identification of critical regulatory processes involved in arsenic-induced neurodevelopmental effects.