Department of Plant Science, Faculty of Biological Science, Kharazmi University, Tehran, Iran.
Laboratory of Plant Physiology-Department of Biology/Research Centre for Biodiversity and Global Change, Universidad Autónoma Madrid, Darwin 2, ES28049 Madrid, Spain.
J Plant Physiol. 2020 Mar-Apr;246-247:153114. doi: 10.1016/j.jplph.2020.153114. Epub 2020 Jan 15.
Aluminium (Al) water pollution is an increasing environmental problem and comprehensive analysis of toxic responses of aquatic primary producer organisms is imperative. We characterized the antioxidant response of Scenedesmus sp. microalga to Al-induced oxidative stress. After 72 h of exposure to Al (0, 10, and 100 μM) in a modified Bold Basal Medium (pH 5.0), we observed cell aggregation and alterations in the subcellular structure, strong lipid peroxidation and oxidative stress induction (detected with the fluorescent probe 2',7'-dichlorodihydrofluorescein diacetate) in parallel with Al accumulation in cells. At the same time, Al toxicity caused depletion of important macronutrients like Ca, which is important for cell-wall structure. Analysis of antioxidant enzymatic activities in Al-treated Scenedesmus cells revealed that catalase, ascorbate peroxidase, as well as different isoforms of superoxide dismutase were inhibited especially at the highest Al dose (100 μM), cells that accumulated the highest concentration of Al. On the other hand, glutathione reductase activity increased at that Al concentration. Immunodetection after Western-blotting confirmed that only ascorbate peroxidase inhibition was apparently due to a decrease in enzyme levels. However, the inhibition of catalase and activation of glutathione reductase activities seemed related with post-translational modifications in protein function as protein expression decreased or increased, respectively under Al stress. Our results may help to understand toxic mechanisms triggered by Al in freshwater microalgae, which in turn could aid to select suitable biomarkers of Al contamination in aquatic ecosystems.
铝（Al）水污染是一个日益严重的环境问题，因此全面分析水生初级生产者对其毒性的反应至关重要。本研究旨在描述小球藻（Scenedesmus sp.）对铝诱导的氧化应激的抗氧化反应。在改良的 Bold 基础培养基（pH 5.0）中，将小球藻暴露于 Al（0、10 和 100 μM）下 72 小时后，我们观察到细胞聚集和亚细胞结构改变，脂质过氧化和氧化应激诱导（通过荧光探针 2'，7'-二氯二氢荧光素二乙酸酯检测）与细胞内 Al 积累同时发生。与此同时，Al 毒性导致重要的大量营养素如 Ca 的消耗，而 Ca 对细胞壁结构很重要。在 Al 处理的小球藻细胞中分析抗氧化酶活性的结果表明，过氧化氢酶、抗坏血酸过氧化物酶以及超氧化物歧化酶的不同同工酶尤其在最高 Al 剂量（100 μM）下受到抑制，此时细胞积累了最高浓度的 Al。另一方面，在该 Al 浓度下，谷胱甘肽还原酶的活性增加。Western-blotting 免疫检测证实，只有抗坏血酸过氧化物酶的抑制显然是由于酶水平降低所致。然而，过氧化氢酶的抑制和谷胱甘肽还原酶的激活似乎与蛋白功能的翻译后修饰有关，因为在 Al 胁迫下，蛋白表达分别减少或增加。我们的研究结果有助于理解 Al 对淡水微藻引发的毒性机制，这反过来又可以帮助选择水生生态系统中 Al 污染的合适生物标志物。
