Deciphering the molecular pathways underlying di(2-ethylhexyl) phthalate degradation and metabolic adaptation in Alexandrium pacificum

Di(2-ethylhexyl) phthalate (DEHP), a widely used plasticizer, is frequently detected in marine environments, raising significant ecological concerns. Biodegradation of DEHP through marine microalgae represents an eco-friendly strategy for effective pollution abatement in marine environments. This study examined the physiological and molecular responses of the dinoflagellate Alexandrium pacificum under DEHP stress and evaluated its ability to biodegrade DEHP. Following DEHP exposure, A. pacificum exhibited a high capacity for DEHP biodegradation, achieving complete removal (below the detection limit) at environmentally relevant concentrations (≤ 200 μg/L) within 72 h, without detectable adverse effects on growth or photosynthesis. The degradation intermediates of DEHP involved β-oxidation, hydrolysis, de-esterification, and aromatic ring cleavage. Notably, DEHP exposure markedly suppressed paralytic shellfish toxin (PST) biosynthesis in A. pacificum , with concentrations of C1, C2, and GTX5 decreasing by 98.7%, 99.6%, and 98.2%, respectively. Transcriptomic analysis indicated that genes involved in DEHP degradation, such as fadB , hppD , xylG , and lysA , were upregulated, whereas PST biosynthesis genes ( SxtD , SxtL , SxtU ) were downregulated, suggesting that A. pacificum actively metabolizes DEHP while concurrently suppressing toxin production. Overall, this study provides comprehensive molecular insights for DEHP biodegradation by marine microalgae and highlights their capacity for effective PAE removal, contributing to ecological health and global seafood safety.