Biomedical subjects

M K Firestone

Publications and source records attributed to M K Firestone.

21 records · Page 2Linked to original sources

PubMed1978

Pathway of degradation of nitrilotriacetate by a Pseudomonas species.

The pathway of degradation of nitrilotriacetate (NTA) was determined by using cell-free extracts and a 35-fold purification of NTA monooxygenase. The first step in the breakdown was an oxidative cleavage of the tertiary amine by the monooxygenase to form the aldo acid, glyoxylate, and the secondary amine, iminodiacetate (IDA). NTA N-oxide acted as a substrate analog for induction of the monooxygenase and was slowly metabolized by the enzyme, but was not an intermediate in the pathway. No intermediate before IDA was found, but an unstable alpha-hydroxy-NTA intermediate was postulated. IDA did undergo cleavage in the presence of the purified monooxygenase to give glyoxylate and glycine, but was not metabolized in cell-free extracts. Glyoxylate was further metabolized by cell-free extracts to yield CO2 and glycerate or glycine, products also found from NTA metabolism. Of the three bacterial isolates in which the NTA pathway has been studied, two strains, one isolated from a British soil and ours from a Michigan soil, appear to be almost identical.

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PubMed1975

Biodegradation of metal-nitrilotriacetate complexes by a Pseudomonas species: mechanism of reaction.

A nitrilotriacetate (NTA)-degrading Pseudomonas species was shown to degrade Ca, Mn, Mg, Cu, Zn, Cd, Fe, and Na chelates of NTA at nearly equal rates when the appropriate metal concentrations are low enough to avoid toxicity from the freed metal. Ni-NTA, however, was not degraded. When higher concentrations of metal-NTA substrates were used, soil stimulated degradation of Cu, Zn, and Cd complexes, probably as a result of binding toxic freed metals. The metal associated with the NTA substrate does not appear to be transported into the cell, since metals do not accumulate in the cells and the presence of NTA reduces metal toxicity. The data are consistent with the hypothesis that an envelope-associated component, probably a transport protein involved in binding, is responsible for the disassociation of the metal from the NTA. Both soil and this NTA-degrading organism destabilize the metal-NTA complex, which suggests that in the natural environment both would act to limit mobilization of metals as soluble NTA chelates. Crude soluble enzyme preparations degrade Fe-, Mn-, and Na-NTA complexes but not Cu-NTA.

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PubMedDate not supplied

Enhanced phenanthrene biodegradation in soil by slender oat root exudates and root debris.

To investigate the mechanisms by which slender oat (Avena barbata Pott ex Link) enhances phenanthrene biodegradation, we analyzed the impacts of root exudates and root debris on phenanthrene biodegradation and degrader community dynamics. Accelerated phenanthrene biodegradation rates occurred in soils amended with slender oat root exudates as well as combined root debris + root exudate as compared with unamended controls. Root exudates significantly enhanced phenanthrene biodegradation in rhizosphere soils, either by increasing contaminant bioavailability and/or increasing microbial population size and activity. A modified most probable number (MPN) method was used to determine quantitative shifts in heterotrophic and phenanthrene degrader communities. During the first 4 to 6 d of treatment, heterotrophic populations increased in all amended soils. Both root debris-amended and exudate-amended soil then maintained larger phenanthrene degrader populations than in control soils later in the experiment after much of the phenanthrene had been utilized. Thus, root amendments had a greater impact over time on phenanthrene degraders than heterotrophs resulting in selective maintenance of degrader populations in amended soils compared with controls.

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