ABSTRACT:This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment. Keywords: ROS; metallothioneins; glutathion; superoxide dismutase; antioxidant defenceList of abbreviations ALA-D = aminolevulinic acid dehydratase; BNF = β-naphthoflavone; CAT = catalase; GPx = glutathione peroxidise; GR = glutathione reductase; GSH = glutathione; GSSG = glutathione disulphide; GST = glutathione S-transferase; LPO = lipid peroxidation; MDA = malondialdehyde; MTs = metallothioneins; NADPH = nicotinamidadeninedinucleotide phosphate (reduced); ROS = reactive oxygen species; SOD = superoxide dismutase

The aim of study was to evaluate the effect of atrazine exposure (5, 15, 20, and 30 mg·L−1) on common carp and the ability of regeneration. During 96 h exposure we observed abnormal behavior in fish exposed to 20 and 30 mg·L−1. Mortality and histological alterations were noticed only in the group exposed to 30 mg·L−1. Most experimental groups showed significantly (P < 0.05) lower values of haemoglobin, haematocrit, leukocyte, and lymphocyte and significantly higher values of monocytes, segmented and band neutrophile granulocytes, and also metamyelocytes and myelocytes. A significantly lower (P < 0.05) leukocyte count was also recorded in experimental groups (5 and 15 mg·L−1) after recovery period. Statistically significant (P < 0.05) alterations in glucose, total protein, lactate, phosphorus, calcium, and biopterin as well as in activities of ALT, AST, ALP, and LDH were found in most experimental groups. These changes were most apparent in the groups exposed to 20 and 30 mg·L−1. Most of the indices were found to be restored after the 7-day recovery period with the exception of LDH, ALT, and lactate in the group exposed to 15 mg·L−1. Our results showed that atrazine exposure had a profound negative influence on selected indices and also on histological changes of common carp.

Deoxynivalenol (DON), produced by the Fusarium genus, is a major contaminant of cereal grains used in the production of fish feed. The effect of mycotoxin deoxynivalenol on rainbow trout (Oncorhynchus mykiss) was studied using a commercial feed with the addition of DON in a dose of 2 mg/kg feed. The fish (n = 40) were exposed to the mycotoxin for 23 days. The trout were divided into two groups, control and experimental groups. Control groups were fed a commercial feed naturally contaminated with a low concentration of DON (225 μg/kg feed); experimental groups were fed a commercial feed with the addition of DON (1964 μg/kg feed). Plasma biochemical and haematological indices, biometric parameters, and histopathological changes were assessed at the end of the experiment. The experimental groups showed significantly lower values in MCH (P < 0.05). In biochemical indices, after 23-day exposure, a significant decrease in glucose, cholesterol (P < 0.05), and ammonia (P < 0.01) was recorded in the experimental group compared to the control group. Our assessment showed no significant changes in biometric parameters. The histopathological examination revealed disorders in the caudal kidney of the exposed fish. The obtained data show the sensitivity of rainbow trout (O. mykiss) to deoxynivalenol.

ABSTRACT:The aim of the present study was to investigate the impact of copper-based pesticides (at concentrations of copper of 20, 30, 40 and 70 µg/l) on one-year-old common carp (Cyprinus carpio L.) during 28 days of exposure. Abnormal behaviour was observed in fish exposed to 70 µg/l from Day 14. Histological alterations were noticed only in liver in the groups exposed to 40 and 70 µg/l. Significant changes (P ˂ 0.05) in almost all haematological indices were found, especially in the group exposed to the highest concentration of copper (70 µg/l). Biochemical analysis revealed various significant (P ˂ 0.05) differences among the tested groups. Significant differences in copper tissue concentration (P ˂ 0.05) among groups were found in liver, gills and kidney. Among antioxidative enzymes, significant changes were revealed mainly in catalase and glutathione-S-transferase activity (P ˂ 0.05). In gills, metallothionein content increased significantly (P ˂ 0.05) in the group exposed to the highest copper concentration (70 µg/l) compared with the other tested groups, including the control. A significant (P ˂ 0.05) change in total glutathione content was recorded in liver and gills, although the reduced/oxidised ratio was not affected. Oxidative damage to lipids increased significantly (P ˂ 0.05) with increasing copper concentration in liver and kidney. The results demonstrate the deleterious influence of copper on common carp even at low, environmentally relevant concentrations.

ABSTRACT:The aim of this study was to assess the effects of Cyperkill 25 EC (a.i. cypermethrin 250 g/l) on cumulative mortality, growth indices, and ontogenetic development of embryos and larvae of common carp (Cyprinus carpio L.). An early-life stage toxicity test was used. Liver, intestine, kidneys, and gills of surviving larvae were examined, and the activity of the detoxifying and antioxidative enzymes glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), glutathione-S-transferase (GST), as well as lipid peroxidation (TBARS) was determined. Eggs of common carp 24 h post-fertilisation were exposed for 35 days to Cyperkill 25 EC at concentrations of 7.2, 36, 72, 144, and 360 μg/l containing the active ingredient cypermethrin at concentrations of 1.8, 9, 18, 36, and 90 μg/l, respectively. All larvae exposed to concentrations higher than 144 μg/l showed signs of damage after five days and died in the next two days; at concentrations of 72 and 36 μg/l total mortality was observed several days after hatching. Larvae exposed to 7.2 μg/l survived to the end of the test but showed significantly lower growth (P < 0.01) and retarded ontogenetic development compared to controls. Examination of these larvae did not reveal histological changes. Activity of GST, GR, and GPx in the exposed group was significantly lower (P < 0.01), while CAT and TBARS did not show significant differences from controls. Exposure to Cyperkill 25 EC affected hatching and survival at tested concentrations above 7.2 μg/l. Alterations in oxidative stress parameters and retarded growth and ontogenetic development were evident at 7.2 μg/l.