Abstract
Organophosphorus flame retardants (OPFRs) are frequently detected in aquatic environments and can potentially amplify the food chain, posing a potential risk to organisms. Marine invertebrates have primitive nervous systems to regulate behavior, but how they respond to OPFRs that are potentially neurotoxic substances is unclear. This study assessed changes in the feeding behavior of rotifer Brachionus plicatilis exposed to alkyl OPFRs tributyl phosphate (TnBP) (0.376 nM, 3.76 and 22.53 µM) to elucidate the mechanism of behavioral toxicity. TnBP at 22.53 μM reduced the ingestion and filtration rates of rotifers for Chlorella vulgaris and Phaeocystis globosa in a 24-h test and altered rotifer-P. globosa population dynamics in 15-d coculture. Ciliary beat frequency was also reduced, and the expression of genes encoding the cilia axoneme was downregulated. TnBP could inhibit rotifer acetylcholinesterase activity by binding this protein and reduce the expression of the exocytotic membrane protein syntaxin-4, suggesting a disorder in nervous regulation of cilia beat. Moreover, TnBP induced abnormal shape and dysfunction of mitochondria, which caused insufficient energy required for ciliary movement. This study revealed diverse neurotoxicity mechanisms of TnBP, particularly as a potentially competing acetylcholinesterase ligand for aquatic invertebrates. Our research also provides a meaningful reference for OPFR-induced behavioral toxicity assessments.
Published Version
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