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« Previous AbstractPolybrominated Diphenyl Ethers Orally Administration to Mice Were Tansferred to Offspring during Gestation and Lactation with Disruptions on the Immune System    Next AbstractResponses of enzymatic antioxidants and non-enzymatic antioxidants in the cyanobacterium Microcystis aeruginosa to the allelochemical ethyl 2-methyl acetoacetate (EMA) isolated from reed (Phragmites communis) »

Ecotoxicol Environ Saf


Title:Physiological and biochemical effects of allelochemical ethyl 2-methyl acetoacetate (EMA) on cyanobacterium Microcystis aeruginosa
Author(s):Hong Y; Hu HY; Li FM;
Address:"Environmental Simulation and Pollution Control State Key Joint Laboratory, Department of Environmental Science and Engineering, Tsinghua University, Beijing 100084, PR China"
Journal Title:Ecotoxicol Environ Saf
Year:2008
Volume:20071203
Issue:2
Page Number:527 - 534
DOI: 10.1016/j.ecoenv.2007.10.010
ISSN/ISBN:1090-2414 (Electronic) 0147-6513 (Linking)
Abstract:"The physiological and biochemical effects of an allelochemical ethyl 2-methyl acetoacetate (EMA) isolated from reed (Phragmites communis) on bloom-forming cyanobacterium, Microcystis aeruginosa, were investigated. EMA significantly inhibited the growth of M. aeruginosa in a concentration-dependent way. The metabolic indices (represented by esterase and total dehydrogenase activities), the cellular redox status (represented by the level of reactive oxygen species (ROS)), and the oxidative damage index (represented by the content of malondialdehyde (MDA), the product of membrane lipid peroxidation) were used to evaluate the physiological and biochemical changes in M. aeruginosa after EMA exposure. Esterase activity in M. aeruginosa did not change (P>0.05) after 2 h of exposure to EMA, but increased greatly after 24 and 48 h (P<0.05). EMA exposure (>0.5 mg L(-1)) resulted in a remarkable loss of total dehydrogenase activity in M. aeruginosa after 4 h (P<0.01), but an increase after 40 h (P<0.05). EMA caused a great increase in ROS level of the algal cells. At high EMA concentration (4 mg L(-1)), the ROS level was remarkably elevated to 1.91 times as much as that in the controls after 2 h. Increases in the ROS level also occurred after 24 and 48 h. The increase in lipid peroxidation of M. aeruginosa was dependent upon EMA concentration and the exposure time. After 40 h of exposure, the MDA content at 4 mg L(-1) of EMA reached approximately 3.5 times (P<0.01) versus the controls. These results suggest that the cellular structure and metabolic activity of M. aeruginosa are influenced by EMA; the increased metabolic activity perhaps reflects the fact that the resistance of cellular response system to the stress from EMA is initiated during EMA exposure, and the oxidative damage induced by EMA via the oxidation of ROS may be an important factor responsible for the inhibition of EMA on the growth of M. aeruginosa"
Keywords:"Acetoacetates/administration & dosage/*pharmacology Dose-Response Relationship, Drug Esterases/metabolism Lipid Peroxidation/drug effects Malondialdehyde Microcystis/*drug effects/metabolism Oxidative Stress Oxidoreductases/metabolism Pheromones/*pharmaco;"
Notes:"MedlineHong, Yu Hu, Hong-Ying Li, Feng-Min eng Research Support, Non-U.S. Gov't Netherlands 2007/12/07 Ecotoxicol Environ Saf. 2008 Oct; 71(2):527-34. doi: 10.1016/j.ecoenv.2007.10.010. Epub 2007 Dec 3"

 
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