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超累積植物富集鎘的生理生化及分子機制

Physiological, biochemical, and molecular mechanisms of cadmium enrichment in hyperaccumulator plants

  • 摘要: 重金屬鎘(Cd)能夠被植物吸收而影響植物生長發育,并且能通過食物鏈作用進入人體,影響人類身體健康,已引起廣泛關注. 超累積植物可以在高濃度Cd污染土壤中正常生長,采取一系列防御措施,包括生成抗氧化酶、細胞壁結合、液泡隔離以及分泌各種化合物(例如植物螯合肽(PCs)和有機酸(OAs))以結合自由移動的Cd離子,從而最大限度地減少Cd的毒性作用. 此外,超累積植物能夠過表達與防御機制有關的基因緩解Cd脅迫. 為全面了解超累積植物對土壤中Cd的吸收、轉運和積累相關的生理生化機制以及分子機制,本文系統地綜述了植物根系分泌物螯合作用、植物激素作用和轉運蛋白基因過表達的調控作用. 過表達基因除提高吸收轉運效果以外,還影響植物生物量和葉綠素含量、緩解氧化脅迫、促進有機酸合成以及植物根系化合物的分泌. 各種機制之間相互影響,共同維持植物正常生長. 本綜述為今后超累積植物修復Cd污染土壤研究提供新的參考方向和思路.

     

    Abstract: With industrial development, the concentration of heavy metals such as cadmium (Cd), lead (Pb), mercury (Hg), and zinc (Zn) in soil has increased significantly owing to human activities. This poses serious threats to plant growth and human health, garnering widespread concern. Cd, in particular, exhibits high mobility in soil. It is predominantly absorbed by plant roots, transported through the xylem, and accumulated in various organelles and sub-organelles within plants. As a non-essential element for plant growth, Cd is toxic even at low concentrations, affecting plants at morphological, physiological, biochemical, and molecular levels. For example, Cd inhibits seed germination, hinders root elongation, and reduces overall plant height. It enters the chloroplasts, compromising the integrity of the chloroplast membrane system, which leads to decreased chlorophyll content, leaf yellowing, reduced photosynthesis, and, in severe cases, plant death. At the cellular level, Cd induces oxidative stress, triggers lipid peroxidation, and generates excessive reactive oxygen species (ROS). These processes damage cell membrane integrity, disrupt cellular functions, and cause oxidative damage. Through long-term natural selection and environmental adaptation, some plants have developed a high tolerance to Cd, with their above-ground parts capable of accumulating heavy metals at concentrations more than 10 times those of ordinary plants. These plants are known as Cd hyperaccumulators. Hyperaccumulators can thrive in soils contaminated with high Cd concentrations by employing various strategies to mitigate Cd adverse effects. These include confining heavy metals within cell walls, isolating them in vacuoles, and secreting compounds such as phytochelatins (PCs) and organic acids (OAs) to bind free Cd ions and form Cd-chelates, thereby reducing Cd mobility. Specialized transporters facilitate the uptake of Cd ions and Cd-chelates from the soil into the plant, subsequently transporting them to aerial parts and distributing them across organelles and sub-organelles to minimize Cd-induced tissue damage. To counteract oxidative damage caused by ROS, plants produce enzymatic antioxidants (e.g., superoxide dismutase, catalase, peroxidase, glutathione reductase) and non-enzymatic antioxidants (e.g., ascorbate, carotenoids, flavonoids, phenols), which help maintain cellular integrity and support plant function. At the molecular level, hyperaccumulators mitigate Cd stress by enhancing the transcription of calcium ion signaling pathways and hormone-stimulated transcription factors. This enhancement facilitates the expression of various genes across different plant organs, helping to alleviate the stress and toxic effects of Cd. To provide a comprehensive understanding of the physiological, biochemical, and molecular mechanisms underlying the absorption, transport, and accumulation of Cd in hyperaccumulator plants, this paper systematically reviews the role of root exudate chelation, the influence of plant hormones, and the regulation of transporter gene overexpression. Overexpressed genes not only enhance the absorption and transport of Cd but also influence plant biomass, chlorophyll content, antioxidant mechanisms, organic acid synthesis, and root exudate production. These interconnected mechanisms work together to sustain normal plant growth under Cd stress. This review can offer new insights and reference points for future research on hyperaccumulator-based phytoremediation of Cd-contaminated soil.

     

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