Organisms in aquatic environments are exposed to a number of pollutants such as pharmaceutical residues. As such, the aim of the present study is to achieve the Lethal Concentration (LC50) of Povidone-iodine (Betadine) for Cyprinus carpio. To do so, the study employs samples, weighing 4±1 [mean±SD] gr, and carries out an experiment in static condition. Based on OECD instructions, after a period of 4 days under controlled water, the physicochemical factors give the following results: pH= 8-8.3, BOD= 690 mg/l, total hardness= 210 mg, and CaCo3 and temperature= 17±0.1 °C. All fish are acclimatized for 10 days in an aquarium, 60×55×30 cm in size, which included the control group (no toxic concentration) as well as the treated aquariums, with Betadine concentration of 20, 40, 60, 80, 100, 120, 140, 160, 180, 200, 400, and 600 mg/l. LC10, LC20, LC30, LC40, LC50, LC60, LC70, LC80, LC90, and LC95 have been measured for 6, 12, 18, and 24 hours. LC50 24h Betadine for C. carpio has been 158.273 ml/l, showing no mortality after 24 hours (i.e. 48h, 72h, and 96h). Results of the present study suggest that Betadine is practically nontoxic and not irritant at low concentrations for this species and it has a short half-life in aquatic environments.

Atrazine (ATR), a selective herbicide, is consistently used worldwide and has been confirmed to be harmful to the health of aquatic organisms. The release of neutrophil extracellular traps (NETs) is one of the newly discovered antimicrobial mechanisms. Although several immune functions have been analyzed under ATR exposure, the effect of ATR on NETs remains mainly unexplored. In the present study, we treated carp neutrophils using 5 μg/ml ATR and 5 μg/ml ATR combined with 100 nM rapamycin to elucidate the underlying mechanisms and to clarify the effect of ATR on phorbol myristate acetate (PMA)-induced NETs. The results of the morphological observation and quantitative analysis of extracellular DNA and myeloperoxidase (MPO) showed that NETs formation were significantly inhibited by ATR exposure. Moreover, we found that in the NETs process, ATR downregulated the expression of the anti-apoptosis gene B-cell lymphoma-2 (Bcl-2), increased the expression of the pro-apoptosis factors Bcl-2-Associated X (BAX), cysteinyl aspartate specific proteinases (Caspase3, 9), and anti-autophagy factor mammalian target of rapamycin (mTOR), decreased the expression of autophagy-related protein light chain 3B (LC3B) and glucose transport proteins (GLUT1, 4), disturbed the activities of phosphofructokinase (PFK), pyruvate kinase (PKM), and hexokinase (HK) and limited reactive oxygen species (ROS) levels, indicating that the reduced NETs release was a consequence of increased apoptosis and diminished ROS burst, autophagy and down-regulated glycolysis under ATR treatment. Meanwhile, rapamycin restored the inhibited autophagy and glycolysis and thus resisted the ATR-suppressed NETs. The present study perfects the mechanism theory of ATR immunotoxicity to fish and has a certain value for human health risk assessment.

Residues of glyphosate (GLY) are widely detected in aquatic systems, raising potential environmental threats and public health concerns, but the mechanism underlying GLY-induced hepatotoxicity in fish has not been fully elucidated yet. This study was designed to explore the hepatotoxic mechanism using juvenile common carp exposed to GLY for 45 d, and plasma and liver samples were collected at 15 d, 30 d, and 45 d to analyze the assays. First, GLY-induced hepatic damage was confirmed by serum liver damage biomarker and hepatic histopathological analysis. Next, changes in oxidative stress biomarkers, gene expression levels of pro- and anti-inflammatory cytokines, and lipid metabolism-related parameters in collected samples were analyzed to clarify their roles in GLY-induced hepatic damage. Data showed that oxidative stress was an early event during GLY exposure, followed by hepatic inflammatory response. Lipid metabolism disorder was a late event during GLY exposure, as evidenced by overproduced hepatic free fatty acids, enhanced lipogenesis-related gene expression levels, reduced lipolysis-related gene expression levels, and resultant hepatic lipid accumulation. Collectively, these findings demonstrate that GLY induces hepatotoxicity in fish through involvement of oxidative stress, inflammatory response, and lipid metabolism disorder, which are intimately interrelated with each other during GLY exposure.

With increasing demand for aquaculture products, water reuse is likely to increase for aquaculture operations around the world. Herein, wastewater stabilization ponds (WSP) represents low cost and sustainable treatment technologies to reduce nutrients and various contaminants of emerging concern from effluent. In the present study, we examined bioaccumulation of selected pharmaceuticals from several therapeutic classes by two important fish species in aquaculture with different feeding preferences (Cyprinus carpio and Sander lucioperca) and their common prey to test whether species specific accumulation occurs. Forty and nineteen from 66 selected pharmaceuticals and their metabolites were positively found in water and sediment samples, respectively from the representative WSP. After a six-month study, which corresponds to aquaculture operations, fourteen pharmaceuticals and their metabolites were detected (at a frequency of higher than 50% of samples) in at least one fish tissue collected from the WSP. We observed striking differences for species and organ specific BAFs among study compounds. Though muscle tissues consistently accumulated lower levels of the target analytes, several substances were elevated in brain, liver and kidney tissues (e.g., sertraline) of both species. Low residual concentrations of these target analytes in aquaculture products (fish fillets) suggest WSPs are promising to support the water-food nexus in aquaculture.

In this study, we aimed to identify the toxic effects of chlorpyrifos exposure on the tissues of common carp. For this purpose, we evaluated histopathological changes in the brain, gills, liver, kidney, testis, and ovaries after 21 days of chlorpyrifos exposure. Activation of 8-OHdG, cleaved caspase-3, and iNOS were assesed by immunofluorescence assay in chlorpyrifos-exposed brain and liver tissue. Additionally, we measured the expression levels of caspase-3, caspase-8, iNOS, MT1, CYP1A, and CYP3A genes in chlorpyrifos-exposed brain tissue, as well as the expression levels of FSH and LH genes in chlorpyrifos-exposed ovaries, using qRT-PCR. We observed severe histopathological lesions, including inflammation, degeneration, necrosis, and hemorrhage, in the evaluated tissues of common carp after both high and low levels of exposure to chlorpyrifos. We detected strong and diffuse signs of immunofluorescence reaction for 8-OHdG, iNOS, and cleaved caspase-3 in the chlorpyrifos-exposed brain and liver tissues. Furthermore, we found that chlorpyrifos exposure significantly upregulated the expressions of caspase-3, caspase-8, iNOS, and MT1, and also moderately upregulated CYP1A and CYP3A in the brain tissue of exposed carp. We also noted downregulation of FSH and LH gene expressions in chlorpyrifos-exposed ovary tissues. Based on our results, chlorpyrifos toxication caused crucial histopathological lesions in vital organs, induced oxidative stress, inflammation, and apoptosis in liver and brain tissues, and triggered reproductive sterility in common carp. Therefore, we can propose that chlorpyrifos toxication is highly dangerous to the health of common carp. Moreover, chlorpyrifos pollution in the water could threaten the common carp population. Use of chlorpyrifos should be restricted, and aquatic systems should be monitored for chlorpyrifos pollution.

Bisphenol S (BPS) has been widely used as a bisphenol alternative in recent few years. However, with mounting evidence suggesting that the presence of BPS in the environment also poses risks to ecosystems and human health, we decided to use the juvenile common carp (Cyprinus carpio) and its primary macrophages as in vivo and in vitro models to examine if BPS is a safe substitute of BPA. The present study evaluated the immune responses of chronic BPS exposure and their mechanisms of action associated with peroxisome proliferator-activated receptor (PPAR) signaling pathway. Potential oxidative stress and pro-inflammatory effects of BPS exposure were identified in fish liver after 60-day exposure, based on the increased reactive oxygen species (ROS) production, antioxidant capacity, NO production, lipid peroxidation, and induction of inflammatory cytokine expression, as well as acute phase protein levels of C-reactive protein, immunoglobulin M, lysozyme, and complement component 3. Moreover, pparγ, PPAR pathway-associated genes retinoid x receptor α (rxrα) and nuclear factor-κb (nfκb) presented a rough concentration-dependent alteration after BPS exposure. An acute BPS exposure to the isolated primary macrophages from juvenile common carp was performed to help elucidate gene expression patterns of pparγ, rxrα, and nfκb in a typical immune cell model, the results were consistent with what we found in vivo experiments for long-term BPS exposure. Furthermore, with coexposure to BPS and a PPARγ antagonist, the restriction of PPAR signaling pathway significantly inhibited the induction of ROS and the mRNA level of interleukin-1β, confirming the involvement of PPAR pathway in BPS-induced chronic inflammatory stress in liver.

In order to better understand the exposure of aquatic systems to halogenated flame retardant contaminants, the present study investigated a variety of legacy and emerging flame retardants in common carp and largemouth bass collected from 58 stations across Illinois (United States). The data revealed that polybrominated diphenyl ethers (PBDEs) generally dominated the flame retardant residues in Illinois fish. Concentrations of ΣPBDEs (including all detectable PBDE congeners) ranged from 24.7 to 8270 ng/g lipid weight (median: 135 ng/g lw) in common carp and 15–3870 ng/g lw (median: 360 ng/g lw) in largemouth bass. In addition to PBDEs, Dechlorane analogues (i.e. Dec-603, Dec-604, and Chlordane Plus) were also frequently detected. Median concentrations of ΣDechloranes (including all detected Dechlorane analogues) were 34.4 and 23.3 ng/g lw in common carp and largemouth bass, respectively. Other emerging flame retardants, including tetrabromo-o-chlorotoluene (TBCT), hexabromobenzene (HBBZ), 2-ethylhexyltetrabromobenzoate (EH-TBB), and bis(2-ethylhexyl)-3,4,5,6-tetrabromo-phthalate (BEH-TEBP), were also detected in 40–78% of the fish at the monitored stations. Spatial analysis revealed significantly greater PBDE concentrations in fish living in impaired urban streams and lakes compared to those from the impaired agricultural and unimpaired agricultural/urban waters, demonstrating a significant urban influence on PBDE contamination. Future studies and environmental monitoring are recommended to focus on temporal trends of PBDEs and alternative flame retardants, as well as human exposure risks via edible fishes, in the identified Areas of Concern within Illinois.

To develop a test for assessing the immunomodulatory effects of chemical pollutants on fish, we evaluated the effects of dexamethasone on the natural host–pathogen interaction between common carp (Cyprinus carpio) and Aeromonas salmonicida. Carp were exposed to 1mgL−1 dexamethasone for the entire experimental period. One week after the exposure test started, the exposed fish, as well as unexposed fish, were bath-infected with A. salmonicida. One hundred percent mortality was observed in bacteria-infected fish exposed to dexamethasone, whereas no infection-associated mortality was observed in infected fish in the absence of dexamethasone exposure. In a separate experiment, dexamethasone exposure significantly suppressed hemolytic complement activity in bacteria-infected fish. These results clearly indicate that exposure to a high concentration of dexamethasone suppressed the carp immune system and caused subsequent mortality. Thus, this proposed test method is likely to be useful for evaluating the immunomodulatory effects of chemicals in fish.

Uptake and biological effects of synthetic glucocorticoids (GCs) were analyzed using common carp (Cyprinus carpio). Fish were exposed to clobetasol propionate (CP) or clobetasone butyrate (CB) individually or in mixture at 1μgL−1 for 21days. Bioconcentration factor (BCF) of CB was calculated as 100, and BCF of CP was less than 16. No effects were found in fish erythrocyte and leukocyte numbers and serum glucose levels after exposure to the selected GCs. On the other hand, serum concentrations of free amino acids significantly increased in GC-exposed groups. Thus, exposures to synthetic GCs at relatively low concentrations seemed to cause enhancement of protein degradation and subsequent increase of serum free amino acids without a corresponding increase in serum glucose levels, an effect which might be related to partial induction of gluconeogenesis by GC.