In this paper are presented the length and weight growth of carp (Cyprinus carpio L.) from artificial lake Slatino (The Former Yugoslav Republic of Macedonia). Artificial lake Slatino because some recontruction works was whole emplied in 1993. Than all fish population was leaved in the river Mramorechka. Artificial lake Slatino has been stocking with individuals of carp (Cyprinus carpio L.) catch from Lake Ohrid. They are used for reproduction and in first years were used for reparation of the fish fond in artificial lake.

Hydrogen peroxide (H₂O₂), as a common disinfectant, has been extensively used in aquaculture. The toxicity of high ambient H₂O₂ for gills and liver of fish has received attention from many researchers. However, whether H₂O₂ exposure induced brain injury and neurotoxicity has not been reported in fish. Therefore, this study aimed to explore the potential mechanism of H₂O₂ toxicity in brain of common carp via transcriptome analysis and biochemical parameter detection. The fish were exposed to 0 (control) and 1 mM of H₂O₂ for 1 h per day lasting 14 days. The results showed that H₂O₂ exposure caused oxidative damage in brain evidenced by decreased glutathione (GSH), total antioxidant capacity (T-AOC) and nicotinamide adenine dinucleotide (NAD⁺) levels, and increased formation of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Meanwhile, H₂O₂ exposure reduced 5-hydroxytryptamine (5-HT) level, and down-regulated tryptophan hydroxylase 1 (tph1a), tph2, 5-hydroxytryptamine receptor 1A-beta (htr1ab) and htr2b expression in brain. Transcriptome analysis showed that H₂O₂ exposure up-regulated 604 genes and down-regulated 1209 genes in brain. Go enrichment displayed that the differently expressed genes (DEGs) were enriched mainly in cellular process, single-organism process, metabolic process, and biological regulation in the biological process category. Further, KEGG enrichment indicated that H₂O₂ exposure led to dysregulation of neurotransmitter signals including depression of glutamatergic synapse, GABAergic synapse and endocannabinoid signaling. Also, we found the alteration of three key pathways including calcium, cAMP and HIF-1 in brain after H₂O₂ exposure. In conclusion, our data indicated that H₂O₂ exposure induced oxidative damage and neurotoxicity, possibly related to dysregulation of neurotransmitters and calcium, cAMP and HIF-1 signaling pathways, which may adversely affect learning, memory and social responses of common carp. This study provided novel insight into biological effects and underlying mechanism of H₂O₂ toxicity in aquatic animal, and contributed to proper application of H₂O₂ in aquaculture.

Cadmium (Cd) is a toxic heavy metal that can be discharged into water environment through industrial activities, threatening the health of aquatic organisms and humans. MicroRNA (miRNA) plays an important role in the process of autophagy. The purpose of this experiment was to study the mechanism of Cd-induced autophagy in common carp hepatopancreas. We established a Cd poisoning model of common carp and explored ultrastructure, two oxidation indicators, three antioxidant indicators, miR-25-3p, two heat shock proteins (Hsps), and nine autophagy-related genes. The results confirmed that deleterious effect of Cd caused the injury of hepatopancreas and the appearance of hepatopancreas autophagic cells in common carp. At the same time, Cd exposure increased the contents of hydrogen peroxide (H₂O₂) and malonaldehyde (MDA), and decreased the activities of catalase (CAT), superoxide dismutase (SOD), and total antioxidative capacity (T-AOC), meaning that Cd caused oxidative stress via the imbalance between peroxide level and antioxidant capacity. Moreover, exposure to Cd increased mRNA expression of microtubule associated protein-1 light chain 3 beta (LC3-II), Dynein, Beclin 1, autophagy-related gene 5 (Atg5), and autophagy-related gene 12 (Atg12); and decreased mRNA expression of mechanistic target of rapamycin kinase (mTOR), indicating that excess Cd caused autophagy, and AMPK/mTOR/ULK1 signaling pathway took part in autophagy induced by Cd in common carp hepatopancreas. Furthermore, Cd down-regulated miR-25-3p and up-regulated its three target genes (AMPK, ULK1 as well as PTEN), suggesting that miR-25-3p mediated autophagy induced by Cd. In addition, we found that Hsps were activated via the up-regulation of Hsp70 and Hsp90. Moreover, oxidative stress mediated autophagy via Hsps in Cd-treated common carp hepatopancreas and Cd-induced autophagy was time dependent. In summary, miR-25-3p, oxidative stress, and Hsps participated in autophagy caused by Cd in common carp hepatopancreas. This study provided a new idea for the mechanism of Cd-induced autophagy in hepatopancreas.

Heavy metals (HMs) in an aquatic environment mainly affects fish, and thus, fish are convenient pollution bio-indicators. In this study, the toxic effects of HM mixture (chromium (Cr), cadmium (Cd), copper (Cu)) in 0 mg/L to 3.2 mg/L concentration range was investigated in Cyprinus carpio (28 days). HM accumulation, histopathology, oxidative stress, and gut microbial changes were evaluated. HMs accumulated in the order of Cr > Cu > Cd, primarily in the kidneys and finally scales. Reactive oxygen species generation increased in all exposure groups up to day 14, with maximum generation at 3.2 mg/L mixture, which later decreased on day 28 in all. Malondialdehydeand and superoxide dismutase levels increased from day 7 to 28 with increased HM concentrations, while total protein showed an inverse trend. Gill histopathology showed major changes such as uplifted and disintegrated primary lamella, and secondary lamella shortening. The kidneys were characterized by glomerular necrosis, Bowman’s capsule expansion, and tubular space dilatation. Proteobacteria and Firmicutes abundance increased up to 59.4% and 99.16% in 0.8 mg/L and 3.2 mg/L treatment groups, respectively. This study provided a better understanding on the physiology and gut microbiota alteration in C. carpio under multiple HM stress.

Although the toxicity of silver nanoparticles (AgNPs) in aquatic organisms has been extensively investigated, the mechanism by which AgNPs damage membranes remains unclear. This study investigated the toxic effects of a series of sub-lethal concentrations of AgNPs on the membranes of freshwater carp (Cyprinus carpio) gills, based on changes in membrane fatty acid (FA) profile, membrane fluidity, membrane lipid peroxidation, and histopathology. Most of the FAs in fish gill membrane was not significantly affected by exposure to multiple AgNPs concentrations, only few significant changes occurred in some specific FAs species at a high concentration of AgNPs exposure. In particular, high concentrations of AgNPs significantly decreased the proportions of two important long-chain n-3 series polyunsaturated FAs (C20: 5n3, and C22: 6n3), resulting in a decreased ratio of n-3 polyunsaturated FAs to n-6 polyunsaturated FAs (Σn-3UFA/Σn-6UFA). The AgNPs also caused a dose-dependent decrease in fish gill membrane fluidity, increased the level of lipid peroxidation, and inhibited Na+/K+-ATPase enzyme activity. Further histopathological examination revealed that exposure to AgNPs can cause toxic responses in the lamellae, including the thinning of the basement membrane, malformation, and inflammation. Together, the results suggest that the mechanism of AgNPs membrane toxicity involves the oxidization of long-chain omega-3 unsaturated FAs to saturated FAs via lipid peroxidation, resulting in, decreased membrane fluidity and ultimately the destruction of the normal physiological function of the fish gill membrane. The findings contribute significantly to our understanding of nanoparticle-induced membrane toxicity and potential risks in aquatic environments.

A combination of previous studies and the present study indicated species-specific debromination of polybromodiphenyl ethers (PBDEs) in teleost fish. Three situations of debromination were found, namely rapid debromination represented by debromination of BDE 99 to BDE 47 observed in common carp, tilapia, crucian carp, and oscar fish; slow debromination represented by debromination of BDE 99 to BDE 49 observed in the abovementioned fish and rainbow trout, salmon, and snakehead; and no or minor debromination observed in catfish. The results of experiments on cofactors, inhibitors, and substrate competitors indicated that activities of outer ring deiodinase of 3, 3′, 5′-triiodothyronine (type I deiodinase), which cannot be inhibited by 6-propyl-2-thiouracil, were responsible for the rapid debromination, and the outer ring deiodinase of thyroxine (type II deiodinase) regulated the slow debromination. The debromination of BDE 99 to BDE 49 was more common, but occurred at a much lower rate (approximately 100 times lower) than the debromination of BDE 99 to BDE 47. This was because the activity of type II deiodinase was nearly two orders of magnitude lower than that of type I deiodinase in the fish species studied. Further studies on debromination of PBDEs and properties of deiodinase in more species are needed to confirm the hypothesis.

Increasing attention has been devoted to the adverse effects of endocrine disrupting chemicals (EDCs) on aquatic environments, such as water, sediment and sludge. To date, few studies have investigated the bio-accumulative characteristics of EDCs in different tissues of diverse wild freshwater fish species and their combined impacts on human health. Five EDCs were investigated in the muscle, liver, gill and, especially, gonad of three fish species collected from the Xiangjiang River, southern China. Carnivorous Siniperca Chuatsi or omnivorous Cyprinus Carpio accumulated higher contents of bisphenol A (BPA) and estrone than herbivorous Parabramis Pekinensis in muscle. Furthermore, 4-n-nonylphenol and estrone were found at higher levels and more frequently in the liver, implying that the liver played an important role in basic metabolism for accumulation, biotransformation and excretion of EDCs. Highest concentrations of BPA found in the gonad revealed that the BPA may pose a serious threat to the reproductive system of aquatic organisms. The mean liver/muscle concentration ratios of 4-n-nonylphenol, BPA, estrone and 17α-ethynyl estradiol confirmed the prolonged exposure of the fish to these EDCs. In addition, the relationships between the fish sizes and the EDC concentrations analyzed by Pearson correlation analysis implied that the bioaccumulation of diethylstilbestrol and BPA increased with the growth of Parabramis Pekinensis, and there was a balance between the uptake rate and elimination rate of EDCs in Siniperca Chuatsi and Cyprinus Carpio. Most importantly, the cumulative impacts of combined EDCs on human health by fish consumption were evaluated. The total estradiol equivalent quantity of estrogens was higher than that of phenols. Also, based on the results of the Monte-Carlo simulation, the 95th percentile values of the total estimated daily intakes from consuming the three freshwater fish species from the Xiangjiang River were higher than the acceptable daily intake.

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.

In this study, the influence of the co-existence of TiO2 nanoparticles on the speciation of arsenite [As(III)] was studied by observing its adsorption and valence changing. Moreover, the influence of TiO2 nanoparticles on the bioavailability of As(III) was examined by bioaccumulation test using carp (Cyprinus carpio). The results showed that TiO2 nanoparticles have a significant adsorption capacity for As (III). Equilibrium was established within 30 min, with about 30% of the initial As (III) being adsorbed onto TiO2 nanoparticles. Most of aqueous As (III) was oxidized to As(V) in the presence of TiO2 nanoparticles under sunlight. The carp accumulated considerably more As in the presence of TiO2 nanoparticles than in the absence of TiO2 nanoparticles, and after 25-day exposure, As concentration in carp increased by 44%. Accumulation of As in viscera, gills and muscle of the carp was significantly enhanced by the presence of TiO2 nanoparticles. The co-existence of TiO2 nanoparticles could change the speciation of arsenite by adsorption and photo-oxidation, and enhance its bioaccumulation to carp.