Ethyl 2-methyl acetoacetate (EMA) is a novel allelochemical exhibiting inhibitory effects on the growth of marine unicellular alga Phaeodactylum tricornutum (P. tricornutum). Oxidative damage and antioxidant responses in P. tricornutum were investigated to elucidate the mechanism involved in EMA inhibition on algal growth. The increase in reactive oxygen species (ROS) levels and malondialdehyde (MDA) contents following exposure to EMA suggested that alga was suffered from oxidative stress and severely damaged. The decrease in cell activity and cellular inclusions suggested that cell growth was greatly inhibited. The activities of the antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxide (GSH-PX) and glutathione S-transferase (GST) increased with the exposure concentration and decreased with the prolongation of exposure time. Cellular ascorbic acid (AsA) and reduced glutathione (GSH) systems were also involved in resisting oxidative stress of EMA by altering the composition of AsA and GSH pools. EMA exposure increased the contents of AsA, GSH, dehydroascorbate (DAsA) and glutathione (GSSG). However, the regeneration rate of AsA/DAsA did not change obviously between treatments and the control, while that of GSH/GSSG decreased significantly under 14 mmol/L EMA exposure on the 3rd day. These results showed that EMA-induced oxidative damage might be responsible for EMA inhibition on P. tricornutum growth and cellular antioxidant enzymes and non-enzymatic antioxidants were improved to counteract the oxidative stress. (C) 2011 Elsevier Inc. All rights reserved.

中文翻译：

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化感化学 2-甲基乙酰乙酸乙酯 (EMA) 诱导三角褐指藻的氧化损伤和抗氧化反应

Ethyl 2-methyl acetoacetate (EMA) 是一种新型化感化学物质，对海洋单细胞藻类三角褐指藻 (P. tricornutum) 的生长具有抑制作用。研究了三角褐指藻中的氧化损伤和抗氧化反应，以阐明 EMA 抑制藻类生长的机制。暴露于 EMA 后活性氧 (ROS) 水平和丙二醛 (MDA) 含量的增加表明藻类遭受氧化应激并严重受损。细胞活性和细胞内含物的降低表明细胞生长受到极大抑制。抗氧化酶的活性包括超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽还原酶（GR）、过氧化谷胱甘肽（GSH-PX）和谷胱甘肽S-转移酶（GST）随着暴露浓度的增加而增加，随着暴露时间的延长而减少。细胞抗坏血酸 (AsA) 和还原型谷胱甘肽 (GSH) 系统也通过改变 AsA 和 GSH 池的组成参与抵抗 EMA 的氧化应激。EMA 暴露增加了 AsA、GSH、脱氢抗坏血酸 (DAsA) 和谷胱甘肽 (GSSG) 的含量。然而，AsA/DAsA 的再生率在处理和对照之间没有明显变化，而 GSH/GSSG 的再生率在第 3 天在 14 mmol/L EMA 暴露下显着下降。这些结果表明 EMA 诱导的氧化损伤可能是 EMA 对 P. tricornutum 生长和细胞抗氧化酶和非酶抗氧化剂得到改善，以抵消氧化应激。(C) 2011 Elsevier Inc. 保留所有权利。