School of Resources & Environmental Science, Hubei International Scientific and Technological Cooperation Base of Sustainable Resource and Energy, Hubei Key Laboratory of Biomass-Resources Chemistry and Environmental Biotechnology, Wuhan University, Wuhan, 430079, PR China; Zhejiang Province Key Laboratory of Recycling and Ecological Treatment of Waste Biomass, School of Environment and Natural Resources, Zhejiang University of Science & Technology, Hangzhou, Zhejiang 310023, China.
School of Resources & Environmental Science, Hubei International Scientific and Technological Cooperation Base of Sustainable Resource and Energy, Hubei Key Laboratory of Biomass-Resources Chemistry and Environmental Biotechnology, Wuhan University, Wuhan, 430079, PR China.
Environ Pollut. 2024 Sep 15;357:124466. doi: 10.1016/j.envpol.2024.124466. Epub 2024 Jun 27.
Oxidative stress is a universal interpretation for the toxicity mechanism of nanoplastics to microalgae. However, there is a lack of deeper insight into the regulation mechanism in microalgae response to oxidative stress, thus affecting the prevention and control for nanoplastics hazard. The integrated analysis of transcriptomics and metabolomics was employed to investigate the mechanism for the oxidative stress response of Chlorella pyrenoidosa to nanoplastics and subsequently lock the according core pathways and driver genes induced. Results indicated that the linoleic acid metabolism, glycine (Gly)-serine (Ser)-threonine (Thr) metabolism, and arginine and proline metabolism pathways of C. pyrenoidosa were collectively involved in oxidative stress. The analysis of linoleic acid metabolism suggested that nanoplastics prompted algal cells to secrete more allelochemicals, thereby leading to destroy the immune system of cells. Gly-Ser-Thr metabolism and arginine and proline metabolism pathways were core pathways involved in algal regulation of cell membrane function and antioxidant system. Key genes, such as LOX2.3, SHM1, TRPA1, and proC1, are drivers of regulating the oxidative stress of algae cells. This investigation lays the foundation for future applications of gene editing technology to limit the hazards of nanoplastics on aquatic organism.
氧化应激是纳米塑料对微藻毒性机制的一种普遍解释。然而,对于微藻应对氧化应激的调控机制缺乏更深入的了解,从而影响了对纳米塑料危害的预防和控制。本研究采用转录组学和代谢组学的综合分析方法,研究了蛋白核小球藻对纳米塑料氧化应激反应的机制,并锁定了相应的核心途径和诱导的关键基因。结果表明,纳米塑料参与了蛋白核小球藻的亚油酸代谢、甘氨酸(Gly)-丝氨酸(Ser)-苏氨酸(Thr)代谢、精氨酸和脯氨酸代谢途径的氧化应激。亚油酸代谢分析表明,纳米塑料促使藻类细胞分泌更多的化感物质,从而破坏细胞的免疫系统。Gly-Ser-Thr 代谢和精氨酸和脯氨酸代谢途径是藻类调节细胞膜功能和抗氧化系统的核心途径。LOX2.3、SHM1、TRPA1 和 proC1 等关键基因是调节藻类细胞氧化应激的关键基因。本研究为未来基因编辑技术在限制纳米塑料对水生生物危害方面的应用奠定了基础。