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Microorganisms May 2023The accumulation of xenobiotic compounds in different environments interrupts the natural ecosystem and induces high toxicity in non-target organisms. Diclofenac is one...
The accumulation of xenobiotic compounds in different environments interrupts the natural ecosystem and induces high toxicity in non-target organisms. Diclofenac is one of the commonly used pharmaceutical drugs that persist in the environment due to its low natural degradation rate and high toxicity. Therefore, this study aimed to isolate potential diclofenac-degrading bacteria, detect the intermediate metabolites formed, and determine the enzyme involved in the degradation process. Four bacterial isolates were selected based on their ability to utilize a high concentration of diclofenac (40 mg/L) as the sole carbon source. The growth conditions for diclofenac degradation were optimized, and bacteria were identified as (S1), (S2), (S11), and (S18). The highest percentage of degradation was recorded (97.79 ± 0.84) after six days of incubation for S11, as analyzed by HPLC. To detect and identify biodegradation metabolites, the GC-MS technique was conducted for the most efficient bacterial strains. In all tested isolates, the initial hydroxylation of diclofenac was detected. The cleavage step of the NH bridge between the aromatic rings and the subsequent cleavage of the ring adjacent to or in between the two hydroxyl groups of polyhydroxylated derivatives might be a key step that enables the complete biodegradation of diclofenac by S18, as well as S1. Additionally, the laccase, peroxidase, and dioxygenase enzyme activities of the two strains, as well as S1, were tested in the presence and absence of diclofenac. The obtained results from this work are expected to be a useful reference for the development of effective detoxification bioprocesses utilizing bacterial cells as biocatalysts. The complete removal of pharmaceuticals from polluted water will stimulate water reuse, meeting the growing worldwide demand for clean and safe freshwater.
PubMed: 37374947
DOI: 10.3390/microorganisms11061445 -
Scientific Reports Feb 2021Phoma stem canker (caused by the ascomycetes Leptosphaeria maculans and Leptosphaeria biglobosa) is an important disease of oilseed rape. Its effect on endophyte...
Phoma stem canker (caused by the ascomycetes Leptosphaeria maculans and Leptosphaeria biglobosa) is an important disease of oilseed rape. Its effect on endophyte communities in roots and shoots and the potential of endophytes to promote growth and control diseases of oilseed rape (OSR) was investigated. Phoma stem canker had a large effect especially on fungal but also on bacterial endophyte communities. Dominant bacterial genera were Pseudomonas, followed by Enterobacter, Serratia, Stenotrophomonas, Bacillus and Staphylococcus. Achromobacter, Pectobacter and Sphingobacterium were isolated only from diseased plants, though in very small numbers. The fungal genera Cladosporium, Botrytis and Torula were dominant in healthy plants whereas Alternaria, Fusarium and Basidiomycetes (Vishniacozyma, Holtermaniella, Bjerkandera/Thanatephorus) occurred exclusively in diseased plants. Remarkably, Leptosphaeria biglobosa could be isolated in large numbers from shoots of both healthy and diseased plants. Plant growth promoting properties (antioxidative activity, P-solubilisation, production of phytohormones and siderophores) were widespread in OSR endophytes. Although none of the tested bacterial endophytes (Achromobacter, Enterobacter, Pseudomonas, Serratia and Stenotrophomonas) promoted growth of oilseed rape under P-limiting conditions or controlled Phoma disease on oilseed rape cotyledons, they significantly reduced incidence of Sclerotinia disease. In the field, a combined inoculum consisting of Achromobacter piechaudii, two pseudomonads and Stenotrophomonas rhizophila tendencially increased OSR yield and reduced Phoma stem canker.
Topics: Achromobacter; Ascomycota; Brassica napus; Disease Resistance; Endophytes; Mycobiome; Phoma; Plant Diseases; Plant Roots; Stenotrophomonas
PubMed: 33589671
DOI: 10.1038/s41598-021-81937-7