Background:　Tris　(2-chloroethyl)　phosphate　(TCEP),　a　widely　used　flame　retardant,　is　widespread　in　the　environment　and　potentially　harmful　to　organisms.　However,　the　specific　mechanisms　of　TCEP-induced　neurological　and　reproductive　toxicity　in　fish　are　largely　unknown.　Turbot　(Scophthalmus　maximus)　is　cultivated　on　a　large　scale,　and　the　emergence　of　pollutants　with　endocrine　disrupting　effects　seriously　affects　its　economic　benefits.　This　study　aimed　to　investigate　the　toxic　effects　of　TCEP　on　turbot　by　integrating　physio-biochemical　and　transcriptomic　analyses.　Results:　TCEP　exposure　induced　severe　neuroendocrine　disrupting　effects　in　turbot.　Firstly,　the　hormone　levels　of　luteinizing　hormone　(LH),　follicle-stimulating　hormone　(FSH),　estradiol　(E2),　and　11-ketotestosterone　(11-KT)　were　significantly　decreased　under　prolonged　TCEP　stress,　which　may　have　a　negative　impact　on　normal　reproductive　function.　We　identified　and　summarized　representative　differentially　expressed　genes　(DEGs)　and　their　functions,　such　as　endocrine　system　and　oxidative　stress.　Pathway　enrichment　showed　that　the　toxicological　characteristics　of　TCEP　on　turbot　were　neuroendocrine　regulation　disorders,　including　oxidative　phosphorylation,　apoptosis,　steroid　biosynthesis,　GnRH　signaling　pathway　and　so　on.　Weighted　gene　co-expression　network　analysis　(WGCNA)　also　revealed　key　genes　involved　in　these　pathways.　Among　these　genes,　those　encoding　the　components　of　the　electron　transport　chain　presented　an　initial　increase　in　expression　followed　by　a　decrease,　indicating　that　TCEP　stress　might　affect　mitochondrial　function　and　lead　to　cell　damage.　This　finding　was　also　supported　by　the　upregulation　of　apoptosis-related　gene　expression.　Moreover,　acute　exposure　to　TCEP　regulated　MAPK-mediated　transduction　and　regulation　of　GnRH　signaling,　thereby　altering　the　expression　of　hypothalamic-pituitary-gonadal　(HPG)　axis-related　genes.　Conclusions:　These　findings　revealed　the　endocrine　disrupting　effects　of　TCEP　on　turbot　and　identified　biomarkers　related　to　reproductive　toxicity,　providing　early　warning　for　the　monitoring　of　healthy　aquaculture.　©　The　Author(s)　2024.