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Effect of oxygen on the stability and inducibility of the biodegradative capability of benzoate

作者
Özer Çınar,Timur Deniz,C. P. Leslie Grady
出处
期刊:Water Science and Technology [Pergamon Press]
卷期号:48 (8): 247-254 被引量:4
标识
DOI:10.2166/wst.2003.0475
摘要

Anoxic zones in biological nitrogen removal systems are typically open to the atmosphere and receive oxygen from the atmosphere and the recirculation flow from the aerobic zone. This raises the question of how such oxygen input might influence the stability and inducibility of the enzyme systems involved in biodegradation of aromatic compounds. To investigate this, various amounts of oxygen were added to mixed culture denitrifying chemostats receiving benzoate at 667 mg/h as chemical oxygen demand (COD), and the stability and inducibility of the culture's benzoate biodegradative capability (BBC) were tested in aerobic and anoxic fed-batch reactors (FBRs). Cultures from chemostats receiving oxygen at 0, 33, 133, 266, and 466 mg O2/h lost almost all of their anoxic BBC within one hour after being transferred to an aerobic FBR and the first three cultures did not recover it upon being returned to anoxic conditions. The last two cultures recovered their anoxic BBC between 9 and 16 h during the 16 h aerobic exposure period that preceded their return to anoxic conditions and continued to increase their anoxic BBC as they were retained under anoxic conditions. In contrast, the culture from a chemostat receiving oxygen at 67 mg O2/h retained its anoxic BBC longer, recovered it within 3 h after its return to anoxic conditions, and increased it linearly thereafter. None of the cultures developed any aerobic BBC during the 16 h aerobic exposure period in FBRs. The results suggest that higher oxygen inputs into anoxic reactors helped the mixed microbial cultures recover and/or induced anoxic BBC more easily when they were exposed to alternating aerobic/anoxic environments. The exceptional behavior of the culture from the chemostat receiving oxygen at a rate of 67 mg O2/h may have been caused by the presence of a protective mechanism against the toxic forms of oxygen.

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