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Emerging evidence indicates that N -(1,3-dimethylbutyl)- N ′-phenyl- p -phenylenediamine (6PPD) and its derivative 6PPD-quinone (6PPD-Q) exert photosynthetic toxicity on aquatic macrophytes. However, their precise inhibitory mechanisms and toxic targets within the photosynthetic pathways remain poorly understood. Through a combination of physio-biochemical indicators, multiomics analysis, and molecular docking simulation, this study systematically explored the photosynthetic toxic effects of 6PPD and 6PPD-Q on Ceratophyllum demersum L. ( C. demersum ). Transcriptomic data identified photosynthetic antenna proteins as primary molecular targets, with both contaminants perturbing the transcriptional regulation of genes and impairing the structural plasticity of associated proteins. These molecular perturbations consequently disrupted the photosynthetic electron transport efficiency. Metabolomic evidence revealed subsequent carbohydrate metabolism imbalances, suggesting compromised carbon fixation capacity of C. demersum . Additionally, molecular docking simulations demonstrated superior binding affinities for both compounds with antenna proteins, particularly emphasizing the enhanced interactions mediated by 6PPD-Q’s quinone structure. Comparative analysis indicated that 6PPD-Q’s structural modifications may confer greater photosynthetic toxicity compared to the parent compound 6PPD. This multiomics investigation reveals the mechanistic basis of 6PPD and 6PPD-Q-driven photosynthetic toxicity and underscores their potential to destabilize aquatic ecosystems by disrupting primary productivity.
Li et al. (Thu,) studied this question.