Chen Xiao-Dong, Liu Yue, Yang Li-Ming, Hu Xiang-Yang, Jia Ai-Qun
School of Life and Pharmaceutical Sciences, State Key Laboratory of Marine Resource Utilization in South China Sea, Hainan University, Haikou, China.
School of Environmental and Biological Engineering, Nanjing University of Science and Technology, Nanjing, China.
Front Plant Sci. 2020 Jul 17;11:1105. doi: 10.3389/fpls.2020.01105. eCollection 2020.
Cyanobacterial blooms have become more frequent and serious in recent years. Not only do massive blooms cause environmental pollution and nutrient eutrophication, but they also produce microcystins (MCs), a group of toxic cycloheptapeptides, which threaten aquatic ecosystem and human health. As such, clarifying the allelopathic interactions between cyanobacteria and other algae is critical to better understand the driving factors of blooms. To date, however, such studies remain largely insufficient. Here, we treated model alga with microcystin-LR (MC-LR) to determine its allelopathic effects. Results showed that MC-LR markedly suppressed cell viability. Comparative proteomic and physiological analyses revealed that MC-LR significantly up-regulated protein abundance of antioxidants ascorbate peroxidase (APX) and catalase (CAT) at the beginning stage of exposure. This was accompanied by an over-accumulation of hydrogen peroxide (HO), suggesting that MC-LR suppresses cell viability oxidative damage. Furthermore, we found that MCs induced desulfhydrase (DES) activity for hydrogen sulfide (HS) generation at the beginning stage. Additional HS donors reactivated antioxidant enzyme activity, which reduced HO accumulation and ultimately enhanced tolerance to MC-LR damage. This effect could be reserved by inhibiting HS biosynthesis. Simultaneously, we found that HS also suppressed MC-LR-induced cell autophagy, and thus attenuated the toxic effects of MC-LR. Our findings suggest that oxidative bursts may be the main reason for the allelopathic effects of MC-LR on viability and that HS signaling may enhance tolerance to MC-LR through the activation of antioxidant enzyme activity and suppression of cell autophagy.
近年来，蓝藻水华现象愈发频繁且严重。大规模的水华不仅会造成环境污染和营养物质富营养化，还会产生微囊藻毒素（MCs），这是一类有毒的环七肽，威胁着水生生态系统和人类健康。因此，阐明蓝藻与其他藻类之间的化感相互作用对于更好地理解水华的驱动因素至关重要。然而，迄今为止，此类研究仍十分不足。在此，我们用微囊藻毒素-LR（MC-LR）处理模式藻以确定其化感作用。结果表明，MC-LR显著抑制细胞活力。比较蛋白质组学和生理学分析显示，在暴露初期，MC-LR显著上调抗氧化剂抗坏血酸过氧化物酶（APX）和过氧化氢酶（CAT）的蛋白质丰度。与此同时，过氧化氢（HO）过度积累，这表明MC-LR通过氧化损伤抑制细胞活力。此外，我们发现MCs在暴露初期诱导脱硫酶（DES）活性以产生硫化氢（HS）。额外的HS供体可重新激活抗氧化酶活性，减少HO积累，最终增强对MC-LR损伤的耐受性。抑制HS生物合成可消除这种作用。同时，我们发现HS还抑制MC-LR诱导的细胞自噬，从而减弱MC-LR的毒性作用。我们的研究结果表明，氧化爆发可能是MC-LR对细胞活力产生化感作用的主要原因，而HS信号可能通过激活抗氧化酶活性和抑制细胞自噬来增强对MC-LR的耐受性。
