Abstract：
High concentrations of copper can pollute coastal waters, primarily from agricultural runoff and mining activities, which can harm marine organisms, including seagrasses. The molecular mechanism of copper toxicity to seagrass currently remains unclear. To determine the response to copper, physiological and multi-omic analyses were conducted to explore the molecular mechanism by which copper affects the global threatened seagrass Halophila beccarii Asch. Excessive copper stress causes oxidative damage and stimulates the activity of the antioxidant enzyme system to remove excess reactive oxygen species (ROS), thereby reducing the damage caused by copper stress. Cu increases the activities of superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), peroxidase (EC 1.11.1.7), ascorbate peroxidase (EC 1.11.1.11), glutathione peroxidase (EC 1.11.1.9), ascorbate oxidase (EC 1.10.3.3), glutathione reductase (EC 1.6.4.2), and dehydroascorbate reductase (EC 1.8.5.1) and the content of malondialdehyde and reduces the activity of monodehydroascorbate reductase (EC 1.6.5.4). Under copper stress, H. beccarii upregulates the metabolic pathways of steroid biosynthesis and cutin, suberin, and wax biosynthesis, downregulates the metabolic pathways of arginine and proline metabolism and fructose and mannose metabolism; the levels of expression of the ribosome-related genes; upregulates the levels of expression of circadian rhythm-related proteins and downregulates the levels of glutathione metabolism and the proteins related to carbon fixation. This study provides new insights into the response of seagrass to copper stress and reports potential candidate metabolites, genes, and proteins that can be considered as biomarkers to improve the protection and management of seagrass meadows.
摘要：
高浓度的铜会污染沿海水域，主要来自农业径流和采矿活动，会伤害海洋生物，包括海草。铜对海草毒性的分子机制目前尚不清楚。为了确定对铜的反应，进行了生理和多维分析，以探索铜影响全球受威胁的海草HalophilabeccariiAsch的分子机制。过度的铜胁迫引起氧化损伤并刺激抗氧化酶系统的活性以去除过量的活性氧（ROS），从而减少铜应力造成的损伤。Cu增加超氧化物歧化酶的活性（EC1.15.1.1），过氧化氢酶（EC1.11.1.6），过氧化物酶（EC1.11.1.7），抗坏血酸过氧化物酶（EC1.11.1.11），谷胱甘肽过氧化物酶（EC1.11.1.9），抗坏血酸氧化酶（EC1.10.3.3），谷胱甘肽还原酶（EC1.6.4.2），和脱氢抗坏血酸还原酶（EC1.8.5.1）和丙二醛的含量，并降低单脱氢抗坏血酸还原酶（EC1.6.5.4）的活性。在铜应力下，H.beccarii上调类固醇生物合成和角质的代谢途径，suberin,和蜡的生物合成，下调精氨酸和脯氨酸代谢以及果糖和甘露糖代谢的代谢途径；核糖体相关基因的表达水平；上调昼夜节律相关蛋白的表达水平，并下调谷胱甘肽代谢和与碳固定相关的蛋白的水平。这项研究为海草对铜胁迫的反应提供了新的见解，并报告了潜在的候选代谢物，基因，和可被视为生物标志物的蛋白质，以改善海草草甸的保护和管理。
