Environmental risks and cytotoxic effects of the organophosphorus flame-retardant tris (2-chloroethyl) phosphate (TCEP) on aquatic organisms: An assessment using the Artemia model.

Abstract

Tris (2-chloroethyl) phosphate (TCEP) is a widespread chlorinated organophosphate flame retardant, yet its biological impacts on saline aquatic biota remain largely undefined. Using the brine shrimp Artemia parthenogenetica, we examined TCEP toxicity across a concentration spectrum from environmentally relevant (2 µg/L) to acutely lethal levels (48-h LC₅₀ = 641.3 mg/L, 95% CI: 603.5-686.1 mg/L), revealing exceptional native tolerance. At 2 µg/L, no teratogenicity or oxidative damage occurred, though glutathione S-transferase (GST) detoxification genes GstS1 and GstO1 were transcriptionally induced, representing an early molecular perturbation. Across higher exposures (5-200 mg/L), TCEP dose-dependently impaired cyst hatching, provoked severe developmental malformations (up to 44%), and disrupted naupliar swimming. Biochemical assays showed catalase induction at 100-200 mg/L and lipid peroxidation with redox disturbance at 200 mg/L, abnormalities that extended into nauplii as widespread apoptosis. Transcriptomics at 200 mg/L identified 1464 differentially expressed genes enriched in cytochrome P450, RNA polymerase, and glutathione metabolism pathways. qPCR confirmed broad suppression of GST-associated genes (Gst5, Ugt2b14, Gpx3, GstO1) from 5 mg/L, whereas GstD7 exhibited a biphasic response and was ultimately downregulated at 200 mg/L. We propose that TCEP-driven suppression of glutathione-dependent detoxification undermines antioxidant capacity, and despite compensatory catalase upregulation, culminates in oxidative injury, apoptosis, and developmental defect. This work bridges environmental realism and mechanistic depth, providing a foundation for TCEP risk assessment in hypersaline ecosystems.