The pollution of polybrominated diphenyl ethers (PBDEs) is becoming a pressing environmental problem in aquatic environments, and its threat to aquatic organism has received much attention. In this study, Phaeodactylum tricornutum was treated with 0.8 and 4 mg L⁻¹ 2,2′,4,4′-tetrabrominated biphenyl ether (BDE-47), the most toxic PBDEs, for 96 h. BDE-47 inhibited cell growth in a time- and concentration-dependent manner. Observation of cell ultrastructure suggested the damage of the chloroplasts morphology. BDE-47 also decreased the chlorophyll content and the oxygen evolution rate, and altered the performance of photosystems. Transcriptomic analysis revealed differential expression of 62 genes related to photosynthesis in BDE-47 treatments (4 mg L⁻¹) and transcription suppression of 58 genes involved in chlorophyll synthesis, antenna proteins, oxygen evolution, electron transport and downstream carbon fixation, implying potential toxicity targets in cells. Additionally, the levels of reactive oxygen species (ROS) and lipid peroxidation increased under BDE-47 stress and were positively correlated with photosynthesis inhibition. Pretreatment with the ROS scavenger N-acetyl-l-cysteine reduced the extent of inhibition, suggesting that ROS was responsible for these effects. Another experiment with the electron transport chain inhibitor 3-(3,4-dichlorophenyl)-1,1-dimethylurea showed that the generation of ROS was partially blocked, primarily indicating that photosynthetic inhibition induced by BDE-47 contributed to ROS overproduction. Thus, BDE-47 inhibited the photosynthesis by down-regulating the gene expression. This change stimulated ROS production, further leading to chloroplast membrane damage to aggravate this inhibition via a feedback loop. These effects of BDE-47 had adverse outcomes on the entire physiological state and the population growth of the microalgae.

多溴二苯醚（PBDEs）的污染正成为水生环境中迫切的环境问题，其对水生生物的威胁已引起广泛关注。在这项研究中，用0.8和4 mg L ^-1毒性最高的PBDEs L ^-1 2,2'，4,4'-四溴代联苯醚（BDE-47）处理了三角藻（Phaeodyylum tricornutum）96小时。BDE-47以时间和浓度依赖性方式抑制细胞生长。细胞超微结构的观察表明叶绿体形态的损害。BDE-47还降低了叶绿素含量和氧气释放速率，并改变了光系统的性能。转录组分析显示BDE-47处理中与光合作用相关的62个基因的差异表达（4 mg L ^-1）和58种基因的转录抑制，这些基因参与叶绿素合成，触角蛋白，氧气释放，电子转运和下游碳固定，这暗示着细胞中潜在的毒性靶标。此外，在BDE-47胁迫下，活性氧（ROS）和脂质过氧化的水平增加，并且与光合作用抑制呈正相关。用ROS清除剂N-乙酰基-l预处理-半胱氨酸降低了抑制程度，表明ROS负责这些作用。使用电子传输链抑制剂3-（3,4-二氯苯基）-1,1-二甲基脲进行的另一项实验表明，ROS的生成被部分阻止，主要表明BDE-47诱导的光合作用抑制导致ROS的过度生产。因此，BDE-47通过下调基因表达来抑制光合作用。这种变化刺激了ROS的产生，进一步导致叶绿体膜受损，并通过反馈回路加剧了这种抑制作用。BDE-47的这些作用对微藻的整个生理状态和种群增长均产生不利影响。