OBJECTIVES: The aim of this study is to assess the toxicity of PAX-18 in different developmental stages of common carp (Cyprinus carpio). The preparation PAX-18, with its active ingredient polyaluminium chloride (9% of Al), is a coagulation agent that is used mainly to precipitate phosphates, to prevent surface water eutrophication and incidences of cyanobacteria. It is applied to the water environment and thus could present a potential risk to fish. DESIGN: The toxicity tests were performed on common carp according to OECD (203, 210) methodologies. The acute toxic effect was evaluated for juveniles and the early development stage effect was observed in embryo-larval toxicity tests. The results of the toxicity tests (the number of dead individuals at particular test concentrations) were subjected to a probit analysis using an EKO-TOX 5.2 programme to determine the LC50 values of PAX-18. RESULTS: Acute toxicity value expressed as 96hLC50 was 753.1 +/- 24.3 mg.l-1 (67.8 mg.l-1 Al). Effect on early development stage expressed as the no observed effect concentration was 10 mg.l-1 (0.9 mg.l-1 Al), the lowest observed effect concentration was 50 mg.l-1 (4.5 mg.l-1 Al). No significant effects of the preparation PAX-18 in concentrations of 50 mg.l-1 of PAX-18 and lower were found on hatching, length and weight parameters, morphology and histopathology. CONCLUSION: The lethal concentration of PAX-18 found in acute toxicity tests on common carp was 7-14 times higher than the concentration which is usually applied to water (5-10 mg.l-1 Al). Moreover, fish in eutrophicated water sources are exposed to PAX-18 concentrations corresponding with the lowest observed effect concentration only for a short time, therefore the effect on them can be considered as minimal.
- MeSH
- Anti-Bacterial Agents toxicity MeSH
- Aluminum Hydroxide administration & dosage toxicity MeSH
- Carps embryology growth & development MeSH
- Polymers administration & dosage toxicity MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
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.
- MeSH
- Endocrine Disruptors toxicity MeSH
- Liver drug effects metabolism pathology MeSH
- Fatty Acids, Monounsaturated toxicity MeSH
- Kidney drug effects metabolism pathology MeSH
- Oncorhynchus mykiss blood metabolism MeSH
- Oxidative Stress drug effects MeSH
- Lipid Peroxidation drug effects MeSH
- Fish Proteins blood MeSH
- Tetrahydronaphthalenes toxicity MeSH
- Vitellogenins blood MeSH
- Dose-Response Relationship, Drug MeSH
- Gills drug effects metabolism pathology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- MeSH
- Antioxidants MeSH
- Pharmacology MeSH
- Lipid Peroxidation MeSH
- Fishes MeSH
- Research MeSH
- Water Pollution MeSH
- Publication type
- Evaluation Study MeSH
OBJECTIVES: Ketoprofen is a common human medicine from a class of non-steroidal anti-inflammatory drugs (NSAIDs), which is provably detected in surface waters in concentrations ordinarily in μg.L-1. The aim of this study was to compare the acute toxicity of ketoprofen to embryonic and juvenile stages of aquarium fish - zebrafish (Danio rerio). METHODS: Tests were performed according to the methods of the Organisation for Economic Co-operation and Development (OECD) No. 203 (Fish, acute toxicity test) and OECD No. 212 (Fish, short-term toxicity test on embryo and sac-fry stages). RESULTS: The results showed (mean ± SD) LC50 value of ketoprofen to be 632.30 ± 10.10 mg.L-1 in juvenile zebrafish and 6.44 ± 2.22 mg.L-1 in embryonic stages of zebrafish. The results revealed statistically significantly higher sensitivity (p<0.01) of the embryonic stages of zebrafish to ketoprofen compared to its juveniles. The susceptibility of embryos depends on many factors, especially yet improperly developed enzymatic system in embryos, different ways of the absorption of the substance into the organism or differences in metabolism pathways. CONCLUSIONS: The acute toxicity of ketoprofen for juvenile stages of zebrafish is low, but the substance seems to be toxic for embryonic stages.
- MeSH
- Anti-Inflammatory Agents, Non-Steroidal adverse effects toxicity MeSH
- Zebrafish embryology growth & development MeSH
- Embryo, Nonmammalian MeSH
- Cyclooxygenase Inhibitors adverse effects toxicity MeSH
- Ketoprofen adverse effects toxicity MeSH
- Lethal Dose 50 MeSH
- Cell Membrane Permeability drug effects physiology MeSH
- Drug Evaluation, Preclinical MeSH
- Life Cycle Stages drug effects physiology MeSH
- Toxicity Tests, Acute MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
OBJECTIVES: The aim of the study was to investigate effects of the fungicide formulation Spartakus (prochloraz 450 g.L-1) on common carp Cyprinus carpio through biometric, biochemical, haematological and antioxidant indices, induction of xenobiotic metabolizing enzymes and histological examination of selected tissues. DESIGN: The test was performed on juvenile fish, which was exposed to Spartakus (concentrations of prochloraz: 0.05; 0.15 and 0.38 mg.L-1) for 28 days. Haematological indices were assessed using unified methods of haematological examination in fish. Plasma biochemical indices were determined by biochemical analyzer. Concentration of total cytochrome P450 (CYP), glutathione (GSH) content and glutathione-S-transferase (GST) activity were determined spectrophotometrically in hepatopancreas. Activity of liver ethoxyresorufin-O-deethylase (EROD) activity was measured spectrofluorimetrically. Ferric reducing ability of plasma (FRAP) and ceruloplasmin activity were assessed spectrophotometrically. Histological changes in samples of hepatopancreas, skin, gills, spleen, head kidney and caudal kidney were examined by light microscopy. RESULTS: There was a significant rise in hepatosomatic index (HSI) (p<0.01), CYP and EROD (p<0.05) of fish exposed to prochloraz of 0.15 and 0.38 mg.L-1 whereas GST was induced by all concentrations tested and GSH by 0.38 mg.L-1 (p<0.05). Red blood cell count decreased significantly (p<0.05) in prochloraz of 0.05 and 0.15 mg.L-1. Plasma potassium increased (p<0.01) in all Spartakus treated groups, a decline in total protein (p<0.05), ALT, Na+ and Ca (p<0.01) was found in fish exposed to prochloraz of 0.38 mg.L-1. Ceruloplasmin activity was elevated (p<0.05) in the highest concentration tested, FRAP declined (p<0.05) in the same group. Histopathological changes in gills were demonstrated in all pesticide treated groups, with a decreased activity of skin mucous cells in prochloraz of 0.38 mg.L-1. CONCLUSION: The subchronic exposure to Spartakus influenced HSI, induced xenobitic metabolizing enzymes, initiated a disorder of selected plasma indices and a decline in red blood cell count, caused minor histological impairment, and affected antioxidant activities of the test fish.
- MeSH
- Ceruloplasmin metabolism MeSH
- Cytochrome P-450 CYP1A1 metabolism MeSH
- Glutathione metabolism MeSH
- Glutathione Transferase metabolism MeSH
- Imidazoles pharmacology MeSH
- Liver drug effects metabolism MeSH
- Carps metabolism MeSH
- Models, Animal MeSH
- Pancreas drug effects metabolism MeSH
- Fungicides, Industrial pharmacology MeSH
- Cytochrome P-450 Enzyme System metabolism MeSH
- Dose-Response Relationship, Drug MeSH
- Gills drug effects metabolism MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH