Bakkali Y, Ruiz-Santaella J P, Osuna M D, Wagner J, Fischer A J, De Prado R
Department of Agricultural Chemistry and Edaphology, University of Córdoba, 14071 Córdoba, Spain.
J Agric Food Chem. 2007 May 16;55(10):4052-8. doi: 10.1021/jf0624749. Epub 2007 Apr 18.
Fenoxaprop-p-ethyl (FE), 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy] propanoate, ethyl ester (R), is an aryloxyphenoxypropionate herbicide for postemergence control of annual and perennial grasses in paddy fields; its site of action is acetyl-coenzyme A carboxylase (ACCase), an enzyme in fatty acids biosynthesis. The possible mechanism(s) of resistance to FE in a resistant biotype of Echinochloa phyllopogon was examined, namely, absorption, translocation, and metabolism of FE and ACCase susceptibility to fenoxaprop acid (FA). Studies of the in vitro inhibition of ACCase discounted any differential active site sensitivity as the basis of resistance to FE. There were differences in absorption rates between biotypes from 3 to 48 h after application (HAA). Biotypes did not differ in either the amounts or the rates of FE translocated; 98% of applied [14C]FE remaining in the treated leaf. However, there was a good correlation between the rate of herbicide metabolism and the plant resistance. The R biotype produced 5-fold less FA and approximately 2-fold more nontoxic (polar) metabolites 48 HAA than the S biotype. Moreover, the higher rate of GSH conjugation in the resistant biotype as compared to the susceptible one indicates that GSH and cysteine conjugation is the major mechanism of resistance of the R biotype against FE toxicity.
精恶唑禾草灵（FE），2-[4-[(6-氯-2-苯并恶唑基)氧基]苯氧基]丙酸乙酯（R），是一种用于苗后防除稻田一年生和多年生禾本科杂草的芳氧苯氧丙酸类除草剂；其作用位点是脂肪酸生物合成中的一种酶——乙酰辅酶A羧化酶（ACCase）。研究了稗草抗性生物型对FE的可能抗性机制，即FE的吸收、转运和代谢以及ACCase对精恶唑丙酸（FA）的敏感性。体外抑制ACCase的研究排除了任何作为FE抗性基础的差异活性位点敏感性。施药后3至48小时（HAA），不同生物型之间的吸收速率存在差异。不同生物型在FE转运的量或速率上没有差异；施用于处理叶片的[14C]FE中有98%残留。然而，除草剂代谢速率与植物抗性之间存在良好的相关性。在48 HAA时，抗性生物型产生的FA比敏感生物型少5倍，无毒（极性）代谢物多约2倍。此外，与敏感生物型相比，抗性生物型中谷胱甘肽结合率更高，这表明谷胱甘肽和半胱氨酸结合是抗性生物型抵抗FE毒性的主要机制。
