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Photoaged polylactic acid biodegradable microplastics mitigate didecyldimethylammonium chloride toxicity in Microcystis aeruginosa by reducing bioavailability and inducing molecular adaptations
Summary
UV-aged polylactic acid biodegradable microplastics adsorb the biocide DDAC more strongly than virgin PLA particles, reducing its bioavailability to the cyanobacterium Microcystis aeruginosa and activating protective gene expression pathways. This demonstrates that environmental weathering transforms biodegradable microplastics into more active chemical carriers, fundamentally altering the toxicity profile of co-occurring pollutants in aquatic ecosystems.
Despite growing concerns about the ecological risks of biodegradable microplastics (BMPs) in aquatic environments, the combined toxicity of BMPs and coexisting pollutants, particularly to primary producers, remains poorly understood. Quaternary ammonium compounds (QACs), such as didecyldimethylammonium chloride (DDAC), are widespread contaminants that interact readily with BMPs. This study investigated the effects of ultraviolet-induced aging on polylactic acid BMPs (PLA-BMPs) and evaluated the combined toxicity of virgin and aged PLA-BMPs (VPLA and APLA) with DDAC on Microcystis aeruginosa . Aging increased surface roughness, oxidation, and negative charge. Both VPLA and APLA strongly adsorbed DDAC, reducing its bioavailability, with APLA showing a greater effect. DDAC alone induced severe multi-level toxicity to M. aeruginosa , including growth inhibition, photosynthetic impairment, membrane disruption, oxidative stress, and increased microcystin production, while PLA-BMPs alone had negligible toxicity. Co-exposure markedly mitigated DDAC-induced toxicity, especially in the presence of APLA. Transcriptomic analysis revealed that DDAC activated ABC transporters and redox-related pathways, while PLA-BMPs alone elicited minimal responses. Co-exposure induced pronounced molecular adaptations, including the upregulation of genes involved in ABC transporters, O-antigen nucleotide sugar biosynthesis, sulfur and amino acid metabolism, and signal transduction, which collectively limited DDAC internalization and alleviated cytotoxic effects. These findings suggest that PLA-BMPs reduce DDAC toxicity by decreasing bioavailability and activating adaptive molecular responses, providing new insights into the combined toxicity and ecological risks of PLA-BMPs and QACs. • UV aging enhanced DDAC adsorption by increasing surface oxidation and negative charge. • Aged PLA-BMPs reduced DDAC bioavailability more strongly than virgin PLA-BMPs. • DDAC induced severe physiological damage and microcystin release. • Aged PLA-BMPs showed stronger attenuation of DDAC toxicity than virgin PLA-BMPs. • Co-exposure with PLA-BMPs activated ABC transport, metabolic, and signaling pathways.