摘要
The coexistence of antimony (Sb) contamination from textile industries and phosphorus (P) enrichment poses a significant yet understudied threat to aquatic ecosystems. This study elucidates how P availability determines Sb toxicity in cyanobacteria. Under P-deficient conditions (0 and 3.0 mg/L), Sb (50 μg/L) consistently inhibited Synechococcus sp. growth (by 29.5 % and 14.1 %, respectively) over 144 h. While, at optimal and high P levels (5.4 and 9.0 mg/L), Synechococcus sp. cells exhibited initial inhibition followed by growth promotion (by 18.8 % and 38.7 %, respectively). Mechanistically, P-deficient cells accumulated 3.7-fold more Sb, developed severe SOD/CAT imbalance (5.2-fold increase and 44.9 % decrease), and showed substantially higher ROS levels despite rapid initial Sb(III) oxidation. These divergent physiological responses were underpinned by distinct molecular adaptations. Transcriptomic analysis revealed that P-sufficient cells strategically upregulated sulfate transporters while downregulating phosphate transporters (pstS/pstC/pstA) to minimize Sb uptake, exhibited balanced redox regulation, and maintained efficient electron transport chains. In contrast, P-deficient cells upregulated emergency stress responses (flavodoxin FldA) but failed to maintain effective metal transport regulation. This study establishes nutrient status as a key determinant of Sb toxicity, demonstrating that eutrophication transforms Sb from an inhibitor to a promoter, with implications for cyanobacterial bloom management.
危险品化学品经营许可证(带存储)