Polystyrene microparticles can affect the health status of freshwater fish - Threat of oral microplastics intake.

Plastic waste pollution is considered one of the biggest problems facing our planet. The production and use of these materials has led to huge amounts of plastic waste entering the aquatic environment and affecting aquatic life. In our experiment, the effect of polystyrene microparticles (PS-MPs; 52.5 ± 11.5 µm) on individual juvenile rainbow trout (Oncorhynchus mykiss) was tested at three different dietary concentrations of 0.5, 2 and 5 % for six weeks. At the end of the experiment, various health parameters of exposed organisms were compared with the control group. The haematological profile revealed an immune response by a decrease in lymphocyte count with a concurrent increase in the number of neutrophil segments at the highest concentration of PS-MPs (5 %). Biochemical analysis showed significant reductions in plasma ammonia in all tested groups, which may be related to liver and gill damage, as determined by histopathological examination and analysis of inflammatory cytokines expression. In addition, liver damage can also cause a significant decrease in the plasma protein ceruloplasmin, which is synthesized in the liver. PS-MPs disrupted the antioxidant balance in the caudal kidney, gill and liver, with significant changes observed only at the highest concentration. In summary, PS-MPs negatively affect the health status of freshwater fish and represent a huge burden on aquatic ecosystems.

Effects of plastic particles on aquatic invertebrates and fish - A review.

This review summarises the current knowledge on the effects of microplastics and their additives on organisms living in the aquatic environment, particularly invertebrates and fish. To date, microplastics have been recognised to affect not only the behaviour of aquatic animals but also their proper development, causing variations in fertility, oxidative stress, inflammations and immunotoxicity, neurotoxicity, and changes in metabolic pathways and gene expression. The ability of microplastics to bind other xenobiotics and cause combined toxicity along side the effect of other agents is also discussed as well. Microplastics are highly recalcitrant materials in both freshwater and marine environments and should be considered extremely toxic to aquatic ecosystems. They are severely problematic from ecological, economic and toxicological standpoints.

Non-steroidal anti-inflammatory drugs caused an outbreak of inflammation and oxidative stress with changes in the gut microbiota in rainbow trout (Oncorhynchus mykiss).

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.

Do foodborne polyethylene microparticles affect the health of rainbow trout (Oncorhynchus mykiss)?

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.

Could the musk compound tonalide affect physiological functions and act as an endocrine disruptor in rainbow trout?

In the present study, the effect of polycyclic musk compound tonalide (AHTN) in two concentrations was studied in male rainbow trout (Oncorhynchus mykiss, Walbaum 1792). A feeding trial was conducted with AHTN incorporated into feed granules. One concentration was environmentally relevant (854 µg/kg); the second one was 10× higher (8699 µg/kg). The fish were fed twice a day with the amount of feed at 1 % of their body weight. After an acclimatization period, the experimental phase in duration of six weeks followed. At the end of the experiment, fish were sampled and the biometrical data were recorded. Subsequently, hematological and biochemical tests, histopathological examination, analysis of oxidative stress markers and evaluation of endocrine disruption using plasma vitellogenin were performed. In conclusion, an increase of hematocrit for both AHTN concentrations was found, but no significant changes were observed in biochemical profile. Moreover, AHTN caused lipid peroxidation in caudal kidney tissue, which was confirmed by histopathological images. The long-lasting AHTN exposure could thus be harmful for maintaining homeostasis in the rainbow trout organism. However, the vitellogenin concentration seemed not to be affected by AHTN.