Assessment of toxic effects of the antibiotic erythromycin on the marine fish gilthead seabream (Sparus aurata L.) by a multi-biomarker approach
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články
PubMed
30384292
DOI
10.1016/j.chemosphere.2018.10.124
PII: S0045-6535(18)31985-4
Knihovny.cz E-zdroje
- Klíčová slova
- Detoxification, Energy production, Fish, Genotoxicity, Neurotransmission, Oxidative stress,
- MeSH
- antibakteriální látky toxicita MeSH
- biologické markery metabolismus MeSH
- lidé MeSH
- mořan zlatý fyziologie MeSH
- oxidační stres účinky léků MeSH
- peroxidace lipidů účinky léků MeSH
- poškození DNA účinky léků MeSH
- testy toxicity metody MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- antibakteriální látky MeSH
- biologické markery MeSH
Erythromycin (ERY) is one of the most common antibiotics used in human and veterinary practices, leading to ubiquitous environmental distribution and possible toxicity to non-target organisms. The purpose of this study was to determine sub-lethal effects of ERY towards the marine fish Sparus aurata (gilthead seabream). S. aurata were acutely (0.3-323 μg/L, 96 h) and chronically (0.7-8.8 μg/L, 28 d) exposed to ERY. Detoxification [7-ethoxyresorufin O-deethylase (EROD), glutathione S-transferases (GSTs), uridine-diphosphate-glucuronosyltransferase (UGT)], oxidative stress [catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GRed)], lipid peroxidation [thiobarbituric acid reactive substances - (TBARS)], genotoxicity [genetic damage index (GDI) and erythrocytic nuclear abnormalities (ENAs)], neurotransmission [acetylcholinesterase (AChE)] and energy metabolism [lactate dehydrogenase (LDH)] biomarkers were evaluated. Results showed that ERY did not promote significant effects in detoxification biomarkers, but induced slight pro-oxidative effects (decrease of GPx activity in the liver after acute exposure and an increase in gills after chronic exposure; and an increase of hepatic GRed activity following chronic exposure). There was a significant decrease in TBARS after chronic exposure, which contradicts a full scenario of oxidative stress. In terms of genotoxicity, both ERY exposures caused only a significant increase of GDI. Neurotransmission and energy metabolism were not also affected by ERY. Although few toxic effects of ERY have been previously documented (involving different metabolic pathways, as tested in this work), these were mainly observed for freshwater species. These findings suggest low vulnerability of S. aurata to ERY at levels close to the ones found in the wild.
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