Non-steroidal anti-inflammatory drugs caused an outbreak of inflammation and oxidative stress with changes in the gut microbiota in rainbow trout (Oncorhynchus mykiss)
Language English Country Netherlands Media print-electronic
Document type Journal Article
PubMed
35952865
DOI
10.1016/j.scitotenv.2022.157921
PII: S0048-9697(22)05020-3
Knihovny.cz E-resources
- Keywords
- Diclofenac, Gene expression, Histology, Ibuprofen, Microbiome, Toxicity,
- MeSH
- Anti-Inflammatory Agents, Non-Steroidal metabolism MeSH
- Biomarkers metabolism MeSH
- Water Pollutants, Chemical * metabolism MeSH
- Diclofenac metabolism MeSH
- Dysbiosis MeSH
- Ecosystem MeSH
- Disease Outbreaks MeSH
- Ibuprofen metabolism toxicity MeSH
- Oxygen metabolism MeSH
- Pharmaceutical Preparations metabolism MeSH
- RNA, Messenger metabolism MeSH
- Oncorhynchus mykiss * metabolism MeSH
- Oxidative Stress MeSH
- HSP70 Heat-Shock Proteins metabolism MeSH
- Reactive Oxygen Species metabolism MeSH
- Gastrointestinal Microbiome * MeSH
- Water metabolism MeSH
- Inflammation chemically induced MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Anti-Inflammatory Agents, Non-Steroidal MeSH
- Biomarkers MeSH
- Water Pollutants, Chemical * MeSH
- Diclofenac MeSH
- Ibuprofen MeSH
- Oxygen MeSH
- Pharmaceutical Preparations MeSH
- RNA, Messenger MeSH
- HSP70 Heat-Shock Proteins MeSH
- Reactive Oxygen Species MeSH
- Water MeSH
One of the main contributors to pharmaceutical pollution of surface waters are non-steroidal anti-inflammatory drugs (NSAIDs) that contaminate the food chain and affect non-target water species. As there are not many studies focusing on toxic effects of NSAIDs on freshwater fish species and specially effects after dietary exposure, we selected rainbow trout (Oncorhynchus mykiss) as the ideal model to examine the impact of two NSAIDs - diclofenac (DCF) and ibuprofen (IBP). The aim of our study was to test toxicity of environmentally relevant concentrations of these drugs together with exposure doses of 100× higher, including their mixture; and to deepen knowledge about the mechanism of toxicity of these drugs. This study revealed kidneys as the most affected organ with hyalinosis, an increase in oxidative stress markers, and changes in gene expression of heat shock protein 70 to be signs of renal toxicity. Furthermore, hepatotoxicity was confirmed by histopathological analysis (i.e. dystrophy, congestion, and inflammatory cell increase), change in biochemical markers, increase in heat shock protein 70 mRNA, and by oxidative stress analysis. The gills were locally deformed and showed signs of inflammatory processes and necrotic areas. Given the increase in oxidative stress markers and heat shock protein 70 mRNA, severe impairment of oxygen transport may be one of the toxic pathways of NSAIDs. Regarding the microbiota, an overgrowth of Gram-positive species was detected; in particular, significant dysbiosis in the Fusobacteria/Firmicutes ratio was observed. In conclusion, the changes observed after dietary exposure to NSAIDs can influence the organism homeostasis, induce ROS production, potentiate inflammations, and cause gut dysbiosis. Even the environmentally relevant concentration of NSAIDs pose a risk to the aquatic ecosystem as it changed O. mykiss health parameters and we assume that the toxicity of NSAIDs manifests itself at the level of mitochondria and proteins.
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