Yang Yanyan, Li Bingcong, Li Heyang, Wen Huiyu, Qiao Ronghao, Li Ming
College of Natural Resources and Environment, Northwest A&F University, Yangling 712100, Shaanxi, China; College of Resources and Environment, Xinjiang Agricultural University, Urumqi 830052, China.
College of Natural Resources and Environment, Northwest A&F University, Yangling 712100, Shaanxi, China.
Aquat Toxicol. 2025 Sep;286:107472. doi: 10.1016/j.aquatox.2025.107472. Epub 2025 Jun 24.
Revealing the response of aquatic organisms to the toxicity of polycyclic aromatic hydrocarbons (PAHs) from the biological mechanism level is helpful to understanding the aquatic ecological risks of PAHs, and sequentially carrying out the necessary environmental management measures to reduce and eliminate the risks. In the current study, a comprehensive evaluation of the response and protective mechanisms of a widely used subject organism Scenedesmus obliquus to Phenanthrene (PHE) toxicity was conducted, integrating physiological, biochemical, and transcriptomic data. The results demonstrated that cell density, photosynthetic pigment content, and antioxidant enzyme activity in S. obliquus were increased under low concentrations (0.1 mg L) of PHE stress. However, exposure to high concentrations (0.5-10 mg L) of PHE resulted in a decrease in cell density and photosynthetic pigment content, along with significant increases in malondialdehyde (MDA) and reactive oxygen species (ROS) activity, indicating severe lipid peroxidation, cellular damage, and growth inhibition. Transcriptome analysis illustrated that most genes were up-regulated under 0.1 mgL PHE stress, particularly those involved in DNA replication, energy metabolism, and carbohydrate metabolism, suggesting that various metabolic pathways were activated to mitigate the effects of low-concentration PHE stress. Nevertheless, genes associated with the metabolism of energy, carbohydrates, amino acids, and lipids showed negligible expression changes under 10 mg L PHE stress, indicating a suppression of the regulatory mechanisms in S. obliquus. Our findings provided a new insight into the toxicity mechanism of PHE on freshwater microalgae and valuable data for risk assessment of PHE.
从生物机制层面揭示水生生物对多环芳烃（PAHs）毒性的响应，有助于理解PAHs的水生生态风险，并进而采取必要的环境管理措施来降低和消除这些风险。在本研究中，我们综合生理、生化和转录组数据，对广泛使用的受试生物斜生栅藻对菲（PHE）毒性的响应和保护机制进行了全面评估。结果表明，在低浓度（0.1 mg/L）的PHE胁迫下，斜生栅藻的细胞密度、光合色素含量和抗氧化酶活性增加。然而，暴露于高浓度（0.5 - 10 mg/L）的PHE会导致细胞密度和光合色素含量降低，同时丙二醛（MDA）和活性氧（ROS）活性显著增加，表明发生了严重的脂质过氧化、细胞损伤和生长抑制。转录组分析表明，在0.1 mg/L PHE胁迫下，大多数基因上调，特别是那些参与DNA复制、能量代谢和碳水化合物代谢的基因，这表明各种代谢途径被激活以减轻低浓度PHE胁迫的影响。然而，在10 mg/L PHE胁迫下，与能量、碳水化合物、氨基酸和脂质代谢相关的基因表达变化可忽略不计，这表明斜生栅藻的调节机制受到抑制。我们的研究结果为PHE对淡水微藻的毒性机制提供了新的见解，并为PHE的风险评估提供了有价值的数据。
