Effect of ibuprofen on the sulfur autotrophic denitrification process and microbial toxic response mechanism.
Electron transfer
Hormesis effect
Metabolism
Oxidative stress
SAD
Journal
Bioresource technology
ISSN: 1873-2976
Titre abrégé: Bioresour Technol
Pays: England
ID NLM: 9889523
Informations de publication
Date de publication:
Sep 2023
Sep 2023
Historique:
received:
10
03
2023
revised:
28
05
2023
accepted:
30
05
2023
medline:
3
7
2023
pubmed:
6
6
2023
entrez:
5
6
2023
Statut:
ppublish
Résumé
The effect of ibuprofen (IBU) on the sulfur autotrophic denitrification (SAD) process and microbial toxic response mechanism were investigated. Nitrate removal performance was inhibited by high IBU concentrations (10 and 50 mg/L), and the effect of low IBU concentrations (1 mg/L) on nitrate removal performance was negligible. The low IBU concentration induced basal oxidative stress for microbial self-protection, while the high IBU concentration induced high-intensity oxidative stress to damage the microbial cell membrane structure. Electrochemical characterization showed that the low IBU concentration stimulated the electron transfer efficiency, which was inhibited at the high IBU concentration. Moreover, the variation content of nicotinamide adenine dinucleotide (NADH) and nitrate reductase showed that metabolic activity increased at low IBU concentrations and decreased at high IBU concentrations during the sulfur autotrophic nitrate reduction process. This study proposed the hormesis toxic response mechanism of the SAD process to IBU exposure.
Identifiants
pubmed: 37277006
pii: S0960-8524(23)00687-9
doi: 10.1016/j.biortech.2023.129261
pii:
doi:
Substances chimiques
Ibuprofen
WK2XYI10QM
Nitrates
0
Sulfur
70FD1KFU70
Nitrogen
N762921K75
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
129261Informations de copyright
Copyright © 2023 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.