Mechanistic understanding of the toxicity of triphenyl phosphate (TPhP) to the marine diatom Phaeodactylum tricornutum: Targeting chloroplast and mitochondrial dysfunction

摘要

Triphenyl phosphate (TPhP) has been widely detected in various environmental media, including seawater, threatening the survival of marine organisms, especially marine planktic algae that are directly exposed to contamination. However, the hazard potential of TPhP on marine algae has not been studied thoroughly and systematically. In this study, a marine diatom, Phaeodactylum tricornutum, was treated with three concentrations of TPhP (0.08, 0.4 and 0.8 mg/L), and after 24 h of exposure, population growth, ultrastructure, physiology and transcriptome changes were investigated. The results reflected that TPhP suppressed the population growth of algae in a concentration-dependent manner, and the 24-h EC50 value was 1.27 mg/L. At all test concentrations, P. tricornutum could absorb more than 70% of TPhP from seawater over 24 h. Ultrastructural observations suggested a distorted lamellar structure with higher TPhP treatments, and the contents of chlorophyll and its precursors were also altered, as were photosynthetic activities. Moreover, 0.8 mg/L TPhP decreased the mitochondrial membrane potential, induced ROS overproduction and disrupted the cell membrane permeability of algal cells. At the transcriptomic level, some differentially expressed genes were enriched in photosynthetic electron transport, carbon fixation, chlorophyll biosynthesis, the TCA cycle and mitochondrial glycolysis. Additionally, 0.8 mg/L TPhP inhibited lipid de novo biosynthesis, suggesting that it may target organelle membranes, thereby contributing to functional defects. Chloroplasts and mitochondria were interpreted to be the subcellular targets of TPhP in P. tricornutum. These data promote the understanding of the toxic action mode of TPhP toward marine diatoms.