Prasad A R, Dailey H A
Department of Microbiology, University of Georgia, Athens 30602-2605, USA.
Biochem Biophys Res Commun. 1995 Oct 4;215(1):186-91. doi: 10.1006/bbrc.1995.2451.
The diphenyl ether herbicide acifluorfen has been shown to act by inhibition of the terminal enzyme of the protoporphyrin biosynthetic pathway, protoporphyrinogen oxidase (E.C. 1.3.3.4) (PPO), in plant and animal cells. In the present study we show that long term maintenance of murine erythroleukemia (MEL) cells in acifluorfen, which is normally toxic to these cells at 5 microM concentration, results in cells that grow at a near normal rate in 100 microM acifluorfen. Acifluorfen resistant cells do not have increased levels of PPO activity, nor does the PPO made by these cells have increased resistance to acifluorfenin, but these cells accumulate porphyrin and have elevated levels of heme. Data is presented that suggests the resistance of these MEL cells to acifluorfen may be attributable to induction of a cytochrome P450(s).
二苯醚除草剂三氟羧草醚已被证明可通过抑制原卟啉生物合成途径的末端酶——原卟啉原氧化酶（E.C. 1.3.3.4）（PPO），在植物和动物细胞中发挥作用。在本研究中，我们发现，长期将鼠类红白血病（MEL）细胞置于三氟羧草醚中培养（通常在5微摩尔浓度时对这些细胞有毒），会使细胞在100微摩尔三氟羧草醚中以接近正常的速率生长。抗三氟羧草醚的细胞中PPO活性水平并未升高，这些细胞产生的PPO对三氟羧草醚的抗性也未增强，但这些细胞会积累卟啉且血红素水平升高。所呈现的数据表明，这些MEL细胞对三氟羧草醚的抗性可能归因于细胞色素P450的诱导。
