Ahuja Nitina, Singh Harminder Pal, Batish Daizy Rani, Kohli Ravinder Kumar
Department of Botany, Panjab University, Chandigarh, India.
Department of Environment Studies, Panjab University, Chandigarh, India.
Pestic Biochem Physiol. 2015 Feb;118:64-70. doi: 10.1016/j.pestbp.2014.11.012. Epub 2014 Dec 3.
Plant essential oils and their constituent monoterpenes are widely known plant growth retardants but their mechanism of action is not well understood. We explored the mechanism of phytotoxicity of eugenol, a monoterpenoid alcohol, proposed as a natural herbicide. Eugenol (100-1000 µM) retarded the germination of Avena fatua and strongly inhibited its root growth compared to the coleoptile growth. We further investigated the underlying physiological and biochemical alterations leading to the root growth inhibition. Eugenol induced the generation of reactive oxygen species (ROS) leading to oxidative stress and membrane damage in the root tissue. ROS generation measured in terms of hydrogen peroxide, superoxide anion and hydroxyl radical content increased significantly in the range of 24 to 144, 21 to 91, 46 to 173% over the control at 100 to 1000 µM eugenol, respectively. The disruption in membrane integrity was indicated by 25 to 125% increase in malondialdehyde (lipid peroxidation byproduct), and decreased conjugated diene content (~10 to 41%). The electrolyte leakage suggesting membrane damage increased both under light as well as dark conditions measured over a period from 0 to 30 h. In defense to the oxidative damage due to eugenol, a significant upregulation in the ROS-scavenging antioxidant enzyme machinery was observed. The activities of superoxide dismutases, catalases, ascorbate peroxidases, guaiacol peroxidases and glutathione reductases were elevated by ~1.5 to 2.8, 2 to 4.3, 1.9 to 5.0, 1.4 to 3.9, 2.5 to 5.5 times, respectively, in response to 100 to 1000 µM eugenol. The study concludes that eugenol inhibits early root growth through ROS-mediated oxidative damage, despite an activation of the antioxidant enzyme machinery.
植物精油及其单萜成分是广为人知的植物生长抑制剂，但其作用机制尚不清楚。我们探究了丁香酚（一种单萜醇，被提议用作天然除草剂）的植物毒性机制。与胚芽鞘生长相比，丁香酚（100 - 1000 μM）延缓了野燕麦的萌发，并强烈抑制其根系生长。我们进一步研究了导致根系生长抑制的潜在生理和生化变化。丁香酚诱导活性氧（ROS）的产生，导致根系组织中的氧化应激和膜损伤。以过氧化氢、超氧阴离子和羟基自由基含量衡量的ROS生成量，在100至1000 μM丁香酚处理下，分别比对照显著增加了24%至144%、21%至91%、46%至173%。丙二醛（脂质过氧化副产物）增加25%至125%，共轭二烯含量降低（约10%至41%），表明膜完整性受到破坏。在0至30小时的时间段内测量，无论是在光照还是黑暗条件下，表明膜损伤的电解质渗漏均增加。为抵御丁香酚引起的氧化损伤，观察到ROS清除抗氧化酶机制显著上调。响应100至1000 μM丁香酚，超氧化物歧化酶、过氧化氢酶、抗坏血酸过氧化物酶、愈创木酚过氧化物酶和谷胱甘肽还原酶的活性分别提高了约1.5至2.8倍、2至4.3倍、1.9至5.0倍、1.4至3.9倍、2.5至5.5倍。该研究得出结论，尽管抗氧化酶机制被激活，但丁香酚通过ROS介导的氧化损伤抑制早期根系生长。
