Allelochemical ethyl 2-methyl acetoacetate (EMA) induces oxidative damage and antioxidant responses in Phaeodactylum tricornutum

• Published in: Pesticide biochemistry and physiology Vol. 100; no. 1; pp. 93 - 103
• Main Authors: Yang, Cui-Yun, Liu, Su-Jing, Zhou, Shi-Wei, Wu, Hui-Feng, Yu, Jun-Bao, Xia, Chuan-Hai
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.05.2011; Elsevier
• Subjects: Antioxidant enzyme; Biological and medical sciences; Ethyl 2-methyl acetoacetate; Malondialdehyde; Phaeodactylum tricornutum; Reactive oxygen species; Phaeodactylum tricornutum; Reactive oxygen species; Antioxidant enzyme; Malondialdehyde; Ethyl 2-methyl acetoacetate; Oxidative stress; Aliphatic compound; Enzyme; Algae; Biochemical compound; Pesticides; Dialdehyde; Alkanal; Oxidant; Aldehyde; Antioxidant; Allelochemicals; Response; Biological compound; Heterokontophyta; Bacillariophyta; Saturated aliphatic compound; Organic compounds
• ISSN: 0048-3575; 1095-9939
• DOI: 10.1016/j.pestbp.2011.02.014

Antioxidant enzymes including SOD, CAT, GR, GSH-PX and GST of Phaeodactylum tricornutum were triggered by EMA to protect cells from oxidative damage. [Display omitted] ► EMA is a novel allelochemical for controlling marine microalgae. ► EMA exposure results in accumulation of ROS and lipid peroxidation products. ► EMA induces oxidative stress in Phaeodactylum tricormutum. ► Antioxidant enzymes and non-enzymatic antioxidants defend oxidative stress from EMA. 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.