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.
- MeSH
- antiflogistika nesteroidní metabolismus MeSH
- biologické markery metabolismus MeSH
- chemické látky znečišťující vodu * metabolismus MeSH
- diklofenak metabolismus MeSH
- dysbióza MeSH
- ekosystém MeSH
- epidemický výskyt choroby MeSH
- ibuprofen metabolismus toxicita MeSH
- kyslík metabolismus MeSH
- léčivé přípravky metabolismus MeSH
- messenger RNA metabolismus MeSH
- Oncorhynchus mykiss * metabolismus MeSH
- oxidační stres MeSH
- proteiny tepelného šoku HSP70 metabolismus MeSH
- reaktivní formy kyslíku metabolismus MeSH
- střevní mikroflóra * MeSH
- voda metabolismus MeSH
- zánět chemicky indukované MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Due to the fact that plastic pollution is a global environmental problem of modern age, studies on the impact of these synthetic materials on aquatic, and especially fish organisms, are an important part of the ecosystem and human nutrition. In our study, the toxicity of pristine polyethylene (PE) microparticles (approx. 50 μm) on rainbow trout (Oncorhynchus mykiss) was tested in three different dietary concentrations - 0.5%, 2% and 5%. After six weeks of exposure, various health indices were evaluated. Electron microscopy of the intestine revealed the disintegration of PE particles to <5 μm in size, and thus we concluded that microplastics are able to reach tissues. The haematological profile revealed changes in total red blood cells count and haematocrit (5% PE) which could be associated with spleen congestion observed histologically. The marker of lipid peroxidation was increased in gills suggesting the disruption of balance in antioxidant enzymes capacity and histopathological imaging revealed inflammation in higher PE concentrations. In addition, ammonia was decreased and calcium elevated in biochemical profile, confirming the gill damage. Electron microscopy of the gills showed lesions of lamellae and visible rings around the mucinous cell opening indicating their higher activity. Another injured was the liver tissue, as confirmed by hepatodystrophies and increased expression of pro-inflammatory genes in 2% PE. Impaired innate immunity was confirmed by an increased presence of mucinous cells and a decrease in leukocytes. Kidney damage manifested itself by higher expression of pro-inflammatory cytokines and histopathology. The damage in gills, liver and kidney together correlated with the increased antioxidant capacity of plasma. In conclusion, PE microparticles are able to affect health indices of O. mykiss. The potential problem for aquatic ecosystems and even human consumption should be considered.
