Burkholderia cepacia 2a inducibly degraded 2,4-dichlorophenoxyacetate (2,4-D) sequentially via 2,4-dichlorophenol, 3,5-dichlorocatechol, 2,4-dichloromuconate, 2-chloromuconolactone and 2-chloromaleylacetate. Cells grown on nutrient agar or broth grew on 2,4-D-salts only if first passaged on 4-hydroxybenzoate- or succinate-salts agar. Buffered suspensions of 4-hydroxybenzoate-grown cells did not adapt to 2,4-D or 3,5-dichlorocatechol, but responded to 2,4-dichlorophenol at concentrations <0.4 mM. Uptake of 2,4-dichlorophenol by non-induced cells displayed a type S (cooperative uptake) uptake isotherm in which the accelerated uptake of the phenol began before the equivalent of a surface monolayer had been adsorbed, and growth inhibition corresponded with the acquisition of 2.2-fold excess of phenol required for the establishment of the monolayer. No evidence of saturation was seen even at 2 mM 2,4-dichlorophenol, possibly due to absorption by intracellular poly-beta-hydroxybutyrate inclusions. With increasing concentration, 2,4-dichlorophenol caused progressive cell membrane damage and, sequentially, leakage of intracellular K(+), P(i), ribose and material absorbing light at 260 nm (presumed nucleotide cofactors), until at 0.4 mM, protein synthesis and enzyme induction were forestalled. Growth of non-adapted cells was inhibited by 0.35 mM 2,4-dichlorophenol and 0.25 mM 3,5-dichlorocatechol; the corresponding minimum bacteriocidal concentrations were 0.45 and 0.35 mM. Strain 2a grew in chemostat culture on carbon-limited media containing 2,4-D, with an apparent growth yield coefficient of 0.23, and on 2,4-dichlorophenol. Growth on 3,5-dichlorocatechol did not occur without a supplement of succinate, probably due to accumulation of toxic quantities of quinonoid and polymerisation products. Cells grown on these compounds were active towards all three, but not when grown on other substrates. The enzymes of the pathway therefore appeared to be induced by 3,5-dichlorocatechol or some later metabolite. A possible reason is offered for the environmental persistence of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T).

中文翻译：

---

洋葱伯克霍尔德菌2a中2,4-二氯苯氧基乙酸酯降解酶的诱导和代谢中间体的毒性。

洋葱伯克霍尔德菌2a依次通过2,4-二氯苯酚，3,5-二氯邻苯二酚，2,4-二氯粘康酸酯，2-氯粘康内酯和2-氯马来酰乙酸可诱导地降解2,4-二氯苯氧基乙酸酯（2,4-D）。在营养琼脂或肉汤上生长的细胞只有先在4-羟基苯甲酸酯盐或琥珀酸酯盐琼脂上传代时，才在2，4-D盐上生长。4-羟基苯甲酸酯生长的细胞的缓冲悬液不适应2,4-D或3,5-二氯邻苯二酚，但对浓度<0.4 mM的2,4-二氯苯酚有反应。非诱导细胞对2，4-二氯苯酚的吸收显示出S型（协同吸收）等温线，其中加速的苯酚吸收开始于表面单分子层的等价物被吸收之前，而生长抑制则对应于建立单层所需的苯酚过量2.2倍。即使在2 mM 2,4-二氯苯酚下也未见到饱和的迹象，这可能是由于细胞内多聚β-羟基丁酸酯包裹体的吸收。随着浓度的升高，2,4-二氯苯酚会引起进行性细胞膜损伤，并依次引起细胞内K（+），P（i），核糖和吸收260 nm光的材料（假定的核苷酸辅因子）泄漏，直至0.4 mM，阻止蛋白质合成和酶诱导。0.35 mM 2,4-二氯苯酚和0.25 mM 3,5-二氯邻苯二酚可抑制未适应细胞的生长；相应的最低杀菌浓度为0.45和0.35 mM。菌株2a在化学恒温培养中在含2,4-D，表观生长产量系数为0.23的碳限制培养基和2,4-二氯苯酚上生长。增长3，如果不添加琥珀酸酯，则不会发生5-二氯邻苯二酚，这可能是由于有毒量的醌类和聚合产物积聚所致。在这些化合物上生长的细胞对所有这三种都有活性，但在其他底物上生长时则没有活性。因此，该途径的酶似乎是由3,5-二氯邻苯二酚或某些后来的代谢产物诱导的。提供了2,4,5-三氯苯氧基乙酸（2,4,5-T）在环境中的持久性的可能原因。