超累积植物富集镉的生理生化及分子机制

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

  • 摘要: 重金属镉(Cd)能够被植物吸收而影响植物生长发育,并且能通过食物链作用进入人体,影响人类身体健康,已引起广泛关注. 超累积植物可以在高浓度Cd污染土壤中正常生长,采取一系列防御措施,包括生成抗氧化酶、细胞壁结合、液泡隔离以及分泌各种化合物(例如植物螯合肽(PCs)和有机酸(OAs))以结合自由移动的Cd离子,从而最大限度地减少Cd的毒性作用. 此外,超累积植物能够过表达与防御机制有关的基因缓解Cd胁迫. 为全面了解超累积植物对土壤中Cd的吸收、转运和积累相关的生理生化机制以及分子机制,本文系统地综述了植物根系分泌物螯合作用、植物激素作用和转运蛋白基因过表达的调控作用. 过表达基因除提高吸收转运效果以外,还影响植物生物量和叶绿素含量、缓解氧化胁迫、促进有机酸合成以及植物根系化合物的分泌. 各种机制之间相互影响,共同维持植物正常生长. 本综述为今后超累积植物修复Cd污染土壤研究提供新的参考方向和思路.

     

    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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