抄録
We used intact cells and cell extracts to investigate the metabolic pathway of benzoic acid (BA) in Acinetobacter sp. strain ST-1, which dehalogenates 4-chlorobenzoic acid (4-CBA) hydrolytically and then mineralizes it via the β-ketoadipate pathway. Strain ST-1 degraded BA easily, yielding cis, cis-muconic acid and β-ketoadipic acid. A cell extract prepared from cells grown with BA transformed catechol into cis, cis-muconic acid and β-ketoadipic acid, but an extract of cells grown on 4-CBA lacked catechol 1, 2-dioxygenase activity. These results show that BA and 4-CBA are degraded in strain ST-1 by different pathways up to a common intermediate, β-ketoadipic acid, and that BA induces catechol 1, 2-dioxygenase. Therefore, the strain degraded BA via catechol to cis, cis-muconic acid and then to β-ketoadipic acid. The degradation pathways of BA and 4-CBA in strain ST-1 may be linked by the formation of β-ketoadipic acid, and then proceed along the β-ketoadipate pathway, even although the key intermediates before the ring fission are different, namely, catechol for BA and protocatechuic acid for 4-CBA.