Copper induces an oxidative stress condition in the marine alga Ulva compressa that is due to the production of superoxide anions and hydrogen peroxide, mainly in organelles. The increase in hydrogen peroxide is accompanied by increases in intracellular calcium and nitric oxide, and there is a crosstalk among these signals. The increase in intracellular calcium activates signaling pathways involving Calmodulin-dependent Protein Kinases (CaMKs) and Calcium-Dependent Protein Kinases (CDPKs), leading to activation of gene expression of antioxidant enzymes and enzymes involved in ascorbate (ASC) and glutathione (GSH) synthesis. It was recently shown that copper also activates Mitogen-Activated Protein Kinases (MAPKs) that participate in the increase in the expression of antioxidant enzymes. The increase in gene expression leads to enhanced activities of antioxidant enzymes and to enhanced levels of ASC and GSH. In addition, copper induces an increase in photosynthesis leading to an increase in the leve of Nicotinamide Adenine Dinucleotide Phosphate (NADPH). Copper also induces an increase in activities of enzymes involved in C, N, and S assimilation, allowing the replacement of proteins damaged by oxidative stress. The accumulation of copper in acute exposure involved increases in GSH, phytochelatins (PCs), and metallothioneins (MTs) whereas the accumulation of copper in chronic exposure involved only MTs. Acute and chronic copper exposure induced the accumulation of copper-containing particles in chloroplasts. On the other hand, copper is extruded from the alga with an equimolar amount of GSH. Thus, the increases in activities of antioxidant enzymes, in ASC, GSH, and NADPH levels, and in C, N, and S assimilation, the accumulation of copper-containing particles in chloroplasts, and the extrusion of copper ions from the alga constitute essential mechanisms that participate in the buffering of copper-induced oxidative stress in U. compressa.

中文翻译：

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海洋巨藻 Ulva compressa（绿藻门）的铜耐受性、积累和解毒机制：20 年研究。


铜会在海洋藻类石莼中引起氧化应激状态，这是由于超氧阴离子和过氧化氢的产生（主要是在细胞器中）造成的。过氧化氢的增加伴随着细胞内钙和一氧化氮的增加，并且这些信号之间存在串扰。细胞内钙的增加激活涉及钙调蛋白依赖性蛋白激酶 (CaMKs) 和钙依赖性蛋白激酶 (CDPKs) 的信号通路，从而激活抗氧化酶以及参与抗坏血酸 (ASC) 和谷胱甘肽 (GSH) 合成的酶的基因表达。最近的研究表明，铜还能激活丝裂原激活蛋白激酶 (MAPK)，参与抗氧化酶表达的增加。基因表达的增加导致抗氧化酶活性增强以及 ASC 和 GSH 水平提高。此外，铜还能促进光合作用，从而提高烟酰胺腺嘌呤二核苷酸磷酸 (NADPH) 的水平。铜还能诱导参与碳、氮和硫同化的酶活性增加，从而替代因氧化应激而受损的蛋白质。急性暴露中铜的积累涉及谷胱甘肽（GSH）、植物螯合素（PC）和金属硫蛋白（MT）的增加，而慢性暴露中铜的积累仅涉及MT。急性和慢性铜暴露引起叶绿体中含铜颗粒的积累。另一方面，铜与等摩尔量的谷胱甘肽一起从藻类中挤出。 因此，抗氧化酶活性的增加、ASC、GSH 和 NADPH 水平的增加、C、N 和 S 同化的增加、叶绿体中含铜颗粒的积累以及从藻类中排出铜离子是至关重要的。参与缓冲U. compressa 中铜诱导的氧化应激的机制。