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Alleviation of Tris(2-chloroethyl) Phosphate Toxicity on the Marine Rotifer Brachionus plicatilis by Polystyrene Microplastics: Features and Molecular Evidence
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Researchers exposed the marine rotifer Brachionus plicatilis to polystyrene microplastics and the organophosphate flame retardant TCEP in combination, finding that microplastics unexpectedly reversed the growth inhibition and oxidative stress caused by TCEP. Transcriptomic analysis showed upregulation of P-glycoprotein efflux pumps, suggesting microplastics activated detoxification pathways that counteracted TCEP toxicity.
As emerging pollutants, microplastics (MPs) and organophosphorus esters (OPEs) coexist in the aquatic environment, posing a potential threat to organisms. Although toxicological studies have been conducted individually, the effects of combined exposure are unknown since MPs can interact with OPEs acting as carriers. In this study, we assessed the response of marine rotifer, Brachionus plicatilis, to co-exposure to polystyrene MPs and tris(2-chloroethyl) phosphate (TCEP) at different concentrations, including population growth, oxidative status, and transcriptomics. Results indicated that 0.1 μm and 1 μm MPs were accumulated in the digestive system, and, even at up to 2000 μg/L, they did not exert obvious damage to the stomach morphology, survival, and reproduction of B. plicatilis. The presence of 1 μm MPs reversed the low population growth rate and high oxidative stress induced by TCEP to the normal level. Some genes involved in metabolic detoxification and stress response were upregulated, such as ABC and Hsp. Subsequent validation showed that P-glycoprotein efflux ability was activated by combined exposure, indicating its important role in the reversal of population growth inhibition. Such results challenge the common perception that MPs aggravate the toxicity of coexisting pollutants and elucidate the molecular mechanism of the limited toxic effects induced by MPs and TCEP.
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