Most tilapias are microphytes, but some prefer higher plants. Ammonia is one of the most important toxic compounds of nitrogen, which is a serious problem in the environment and aquaculture industry. In the present study, juvenile Oreochromis niloticus were exposed to 10, 20, and 30% (96h LC50) of ammonia for two weeks, which are equivalent to 0.9, 1.8, and 2.7 mg / l, respectively. After this period, the fish were anesthetized and blood samples were taken from the caudal stalk with a heparin syringe for evaluating blood indicators. The tissue samples were taken 0.5 cm from the liver, fixed in 10% formalin buffer, and after dehydration with alcohol, clarification with xylol, blocking with paraffin, and cutting 4-6 microns thick with microtome were done. Finally, the stained slides were studied with a light microscope. The results showed phenomena such as hyperemia, nuclear hypertrophy, sinusoidal dilatation, increased melanomacrophage centers, nucleus margination, hepatocyte vacuolation, and cell necrosis in the liver. In the studies of blood serum factors with the increase of ammonia, it has been increased in  AST, ALT, and ALP compared to the control and other groups. Also, as the ammonia concentration increased, the severity of the lesions also increased. Therefore, ammonia causes changes in the structure and activity of metabolic enzymes of the liver, which must be controlled by creating the appropriate ammonia and management conditions in the aquatic environment.

peer reviewed | Microplastics (MPs) are thought to be ingested by a wide range of marine organisms before being excreted. However, several studies in marine organisms from different taxa have shown that MPs and nanoplastics could be translocated in other organs. In this study, we investigated the presence of MPs in the livers of commercial zooplanktivorous fishes collected in the field. The study focuses mainly on the European anchovy Engraulis encrasicolus but concerns also the European pilchard Sardina pilchardus and the Atlantic herring Clupea harengus. Two complementary methodologies were used to attest the occurrence of MPs in the hepatic tissue and to exclude contamination. 1) MPs were isolated by degradation of the hepatic tissue. 2) Cryosections were made on the livers and observed in polarized light microscopy. Both methods separately revealed that MPs, mainly polyethylene (PE), were translocated into the livers of the three clupeid species. In anchovy, 80 per cent of livers contained relatively large MPs that ranged from 124 μm to 438 μm, showing a high level of contamination. Two translocation pathways are hypothesized: (i) large particles found in the liver resulted from the agglomeration of smaller pieces, and/or (ii) they simply pass through the intestinal barrier. Further studies are however required to understand the exact process. © 2017 Elsevier Ltd

Per- and polyfluoroalkyl substances (PFAS) are ubiquitous in aquatic environments and a recent shift toward emerging PFAS is calling for new data on their occurrence and fate. In particular, understanding the determinants of their bioaccumulation is fundamental for risk assessment purposes. However, very few studies have addressed the combined influence of potential ecological drivers of PFAS bioaccumulation in fish such as age, sex or trophic ecology. Thus, this work aimed to fill these knowledge gaps by performing a field study in the Seine River basin (France). Composite sediment and fish (European chub, Squalius Cephalus) samples were collected from four sites along a longitudinal transect to investigate the occurrence of 36 PFAS. Sediment molecular patterns were dominated by fluorotelomer sulfonamidoalkyl betaines (i.e. 6:2 and 8:2 FTAB, 46% of ∑PFAS on average), highlighting the non-negligible contribution of PFAS of emerging concern. C₉–C₁₄ perfluoroalkyl carboxylic acids, perfluorooctane sulfonic acid (PFOS), perfluorooctane sulfonamide (FOSA) and 10:2 fluorotelomer sulfonate (10:2 FTSA) were detected in all fish samples. Conversely, 8:2 FTAB was detected in a few fish from the furthest downstream station only, suggesting the low bioaccessibility or the biotransformation of FTABs. ∑PFAS in fish was in the range 0.22–3.8 ng g⁻¹ wet weight (ww) and 11–140 ng g⁻¹ ww for muscle and liver, respectively. Fish collected upstream of Paris were significantly less contaminated than those collected downstream, pointing to urban and industrial inputs. The influence of trophic ecology and biometry on the interindividual variability of PFAS burden in fish was examined through analyses of covariance (ANCOVAs), with sampling site considered as a categorical variable. While the latter was highly significant, diet was also influential; carbon sources and trophic level (i.e. estimated using C and N stable isotope ratios, respectively) equally explained the variability of PFAS levels in fish.

Perfluorooctanesulfonic acid (PFOS) is a persistent anthropogenic chemical that can affect the thyroid hormone system in humans and animals. In adults, thyroid hormones (THs) are regulated by the hypothalamic-pituitary-thyroid (HPT) axis, but also by organs such as the liver and potentially the gut microbiota. PFOS and other xenobiotics can therefore disrupt the TH system at various locations and through different mechanisms. To start addressing this, we exposed adult male rats to 3 mg PFOS/kg/day for 7 days and analysed effects on multiple organs and pathways simultaneously by transcriptomics. This included four primary organs involved in TH regulation, namely hypothalamus, pituitary, thyroid, and liver. To investigate a potential role of the gut microbiota in thyroid hormone regulation, two additional groups of animals were dosed with the antibiotic vancomycin (8 mg/kg/day), either with or without PFOS. PFOS exposure decreased thyroxine (T4) and triiodothyronine (T3) without affecting thyroid stimulating hormone (TSH), resembling a state of hypothyroxinemia. PFOS exposure resulted in 50 differentially expressed genes (DEGs) in the hypothalamus, 68 DEGs in the pituitary, 71 DEGs in the thyroid, and 181 DEGs in the liver. A concomitant compromised gut microbiota did not significantly change effects of PFOS exposure. Organ-specific DEGs did not align with TH regulating genes; however, genes associated with vesicle transport and neuronal signaling were affected in the hypothalamus, and phase I and phase II metabolism in the liver. This suggests that a decrease in systemic TH levels may activate the expression of factors altering trafficking, metabolism and excretion of TH. At the transcriptional level, little evidence suggests that the pituitary or thyroid gland is involved in PFOS-induced TH system disruption.

Per- and polyfluorinated alkyl substances (PFAS) are highly persistent chemicals, which pose a potential risk for aquatic wildlife due to their bioaccumulative behaviour and toxicological effects. Although the distribution of PFAS in marine environments has been studied worldwide, little is known on the contamination of PFAS in the southern North Sea. In the present study, the bioaccumulation and trophic transfer of Perfluoroalkyl acids (PFAAs) was studied in liver and muscle tissue of seven fish species and in whole-body tissue of two crustacean species, collected at 10 sites in the Belgian North Sea. Furthermore, the human and ecological health risks were examined. Overall, perfluorooctane sulfonate (PFOS) was predominant in all matrices and other long-chain PFAS were frequently detected. Mean PFOS concentrations ranged from <LOQ to 107 ng/g (ww) in fish liver, from <LOQ to 24 ng/g ww in fish muscle and from 0.29 to 5.6 ng/g ww in crustaceans. Elevated perfluorotridecanoic acid (PFTrDA) concentrations were detected in fish liver from the estuarine and coastal region (<LOQ-116 ng/g ww), indicating a specific point source of this compound. Based on stable isotope analysis, no distinctive trophic transfer patterns of PFAS could be identified which implies that the bioconcentration of PFAS from the surrounding abiotic environment is most likely dominating over the biomagnification in the studied biota. The consumption of commercially important species such as the brown shrimp (Crangon crangon), plaice (Pleuronecta platessa), sole (Solea solea) and whiting (Merlangus merlangus) might pose potential health risks if it exceeds 17 g/day, 18 g/day, 26 g/day and 43 g/day respectively. Most PFOS measurements did not exceed the QSbᵢₒₜₐ,ₕₕ of 9.1 ng/g ww, however, the benchmark of 33 ng/g ww targeting the protection of wildlife from secondary poisoning was exceeded for 43% and 28% of the samples in plaice and sole.

As tricresyl phosphate (TCrP) is commonly found in global water sources, its potential reproductive toxicity to fish is of increasing concern. Japanese medaka larvae were exposed to TCrP at 657.9, 1,511, and 4042 ng/L for 100 days. We identified significant fertilization inhibition (6.9%–12.8%) in all exposure groups. Intersex was significantly induced at 4042 ng/L, with an incidence of 22.0%. TCrP exposure also caused dilation of the efferent duct in the testes with maximum duct widths of 83.3, 93.2, and 149.7 μm in the 657.9, 1,511, and 4042 ng/L exposure groups, respectively. These widths were all significantly larger than that observed in the control group (37.7 μm) and likely contributed substantially to fertilization inhibition. The TCrP metabolites 4-OH-MDTP and 3-OH-MDTP, were detected at high concentrations in the liver and elicited 5.8-fold and 5.3-fold greater androgen receptor antagonistic activity than that elicited by TCrP (39.8 μM), which may explain the intersex observed in low exposure groups. 4-OH-MDTP and 3-OH-MDTP elicited anti-estrogenic activities by blocking the estrogen receptor, and the concentrations at which its responses were equal to the IC₂₀ of tamoxifen were 16.1 μM and 18.9 μM, respectively, as detected using the yeast two-hybrid assay. Such anti-estrogenic activities were likely the main driver of dilation of the efferent duct. Observed adverse outcomes after exposure to TCrP all occurred under environmentally relevant concentrations, suggesting considerable ecological risk to wild fish.

Aqueous film-forming foam (AFFF) has historically contained high concentrations of long-chain per-and polyfluoroalkyl substances (PFAS), which have been linked with adverse health outcomes. However, the toxicity of historical AFFFs remains largely unknown, presenting uncertainties in their risk assessment. This study assessed the toxicity of historical AFFFs by exposing human liver cells (HepG2) to various dilutions of 3M Light Water AFFF or Ansulite AFFF (0.001%, 0.002%, 0.005%, 0.009%, 0.019%, 0.038%, 0.075%, 0.15%, and 0.3%) for 24 h. The effects of the two AFFF formulations on the cell viability, intracellular reactive oxygen species (ROS) production, Nrf2-ARE activity, and DNA damage were assessed by CellTiter 96® Aqᵤₑₒᵤₛ One Solution Cell Proliferation Assay (MTS kit), dichlorofluorescein diacetate assay, luciferase assay, and alkaline Comet assay, respectively. The results revealed that the two brands of AFFFs tested were toxic to HepG2 cells at dilutions lower than the recommended 3% application formulation. Specifically, exposure to 3M Light Water AFFF or Ansulite AFFF induced a dilution-dependent decrease in cell viability, increased intracellular ROS production, and increased Nrf2-ARE activity. However, except for the highest concentration (lowest dilution) of 3M Light Water AFFF tested (0.038%.), both 3M Light Water AFFF and Ansulite AFFF did not significantly induce cellular DNA damage. Overall, 3M Light Water AFFF was more toxic than Ansulite AFFF. The findings from this study provided valuable in vitro toxicity data that may better inform the health risk assessment of these historical AFFFs.

There is a scarcity of studies on the interactions between heavy metals and non-alcoholic fatty liver disease (NAFLD). Using a variety of statistical approaches, we investigated the impact of three common heavy metals on liver enzymes and NAFLD markers in a Korean adult population. We observed that cadmium, mercury, and lead all demonstrated positive correlations with liver enzymes and NAFLD indices. Our findings were mostly robust in secondary analysis, which included three novel mixture modeling approaches (WQS, qgcomp, and BKMR) as well as in silico investigation of molecular mechanisms (genes, miRNAs, biological processes, pathways, and illnesses). The 16 genes interacted with a mixture of heavy metals, which was linked to the development of NAFLD. Co-expression was discovered in nearly half of the interactions between the 18 NAFLD-linked genes. Key molecular pathways implicated in the pathogenesis of NAFLD generated by the heavy metal combination include activated oxidative stress, altered lipid metabolism, and increased cytokines and inflammatory response. Heavy metal exposure levels were related to liver enzymes and NAFLD indices, and cutoff criteria were revealed. More studies are needed to validate our findings and gain knowledge about the effects of chronic combined heavy metal exposure on adult and child liver function and the likelihood of developing NAFLD. To reduce the occurrence of NAFLD, early preventative and regulatory actions (half-yearly screening of workers at high-risk facilities; water filtration; avoiding excessive amounts of seafood, etc.) should be taken.