{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He H"],"funding":["Shanxi 1331 Project","Natural Science Foundation of China","Changzhi Medical College Innovation Team and Key Laboratory of Shanxi Province for Aging Mechanism Research and Transformation","Natural Science Foundation of Shanxi Province, China"],"pagination":["41739"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12647577"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["The environmental pollutant Benzo[a]pyrene (B[a]P) and its ultimate metabolite B[a]P-7,8-diol-9,10-epoxide (BPDE) exhibit neurotoxic effects, yet the underlying molecular mechanisms remain enigmatic. Recently, ferroptosis has emerged as a potential player in B[a]P/BPDE-induced cellular damage. However, whether ferroptosis contributes to B[a]P/BPDE-induced neuron injury remains uncertain. We established a mouse model of learning and memory dysfunction through sub-chronic intragastric administration of B[a]P, with confirmation provided by behavioral alterations and pathological changes in the hippocampus. Furthermore, ferroptosis hallmarks, such as mitochondrial shrinkage, iron and glutamate metabolism disorders, and increased MDA level, were evident. Meanwhile, treatment with 1 mg/kg Ferros"],"journal":["Scientific reports"],"pubmed_title":["Integrated transcriptomics and proteomics reveal ferroptosis induced by B[a]P and BPDE in mouse hippocampal neurons."],"pmcid":["PMC12647577"],"funding_grant_id":["CX202001","202203021211246","30872137","20210302124301","2021-5-2-2-B1"],"pubmed_authors":["Ji T","Li X","Zheng J","Tian F","Ding S","Chen J","Zhou C","Guo X","Lyu Y","He H","Ma Z"],"additional_accession":[]},"is_claimable":false,"name":"Integrated transcriptomics and proteomics reveal ferroptosis induced by B[a]P and BPDE in mouse hippocampal neurons.","description":"The environmental pollutant Benzo[a]pyrene (B[a]P) and its ultimate metabolite B[a]P-7,8-diol-9,10-epoxide (BPDE) exhibit neurotoxic effects, yet the underlying molecular mechanisms remain enigmatic. Recently, ferroptosis has emerged as a potential player in B[a]P/BPDE-induced cellular damage. However, whether ferroptosis contributes to B[a]P/BPDE-induced neuron injury remains uncertain. We established a mouse model of learning and memory dysfunction through sub-chronic intragastric administration of B[a]P, with confirmation provided by behavioral alterations and pathological changes in the hippocampus. Furthermore, ferroptosis hallmarks, such as mitochondrial shrinkage, iron and glutamate metabolism disorders, and increased MDA level, were evident. Meanwhile, treatment with 1 mg/kg Ferros","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-05T19:54:21.898Z","creation":"2026-05-21T03:11:40.792Z"},"accession":"S-EPMC12647577","cross_references":{"pubmed":["41290932"],"doi":["10.1038/s41598-025-26928-8"]}}