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Triazole fungicides are widely used in agriculture that leads to pollution of freshwater ecosystems. The mechanisms of toxicity to fish by the triazole fungicide Topas that contains penconazole (1-[2-(2,4-dichlorophenyl)pentyl]-1H-1,2,4-triazole) have not been studied. The present study aimed to evaluate the effect of goldfish exposure for 96 h to the fungicide Topas at concentrations of 1.5, 15, or 25 mg/L on the plasma and liver biochemical parameters and blood hematological profile. Goldfish exposure to Topas decreased alanine and aspartate transaminase activity and increased lactate dehydrogenase activity in the liver. Plasma lactate dehydrogenase and alanine transaminase activities were elevated in fungicide-treated fish. Topas exposure also enhanced plasma glucose and triacylglycerol concentrations. In the liver, fungicide treatment decreased levels of glucose but elevated triacylglycerols, glycogen, and protein. The results indicate that acute exposure of goldfish to Topas induced strong metabolic perturbations and disruptions of metabolic parameters, suggesting that these could be used to assess sublethal or acute toxic effects of pesticides on aquatic species.

The effects of cool white, natural white, and warm white lights, which have a continuous spectrum throughout the region of surfactant, and blue-red light spectrum on in vitro growth and development of black currant (Ribes nigrum L.) was studied. It was demonstrated that the spectral composition of light affected length and fresh mass of shoots and roots as well as concentrations of chlorophylls, carotenoids, and anthocyanins. The plants grown under warm white light had the longest shoots (2.5 ± 0.2 cm) and fresh mass of shoots (166 ± 12 mg) and roots (80 ± 16 mg) relatively to оne’s grown under other light types. Under blue-red and warm white lights black currant leaves possessed the highest concentrations of chlorophyll a (2.66 ± 0.31 and 2.17 ± 0.14 µmol·gwm-1, respectively), chlorophyll b (1.15 ± 0.15 and 0.87± 0.05 µmol·gwm-1), carotenoids (0.89 ± 0.09 and 0.78 ± 0.05 µmol·gwm-1, respectively) and anthocyanins (1.37 ± 0.20 and 1.09 ± 0.05 µmol·gwm-1, respectively). Thus, blue-red (B:R = 1:4) and warm white lights may be used as an alternative light source for upland black currant culture systems.

Copper is an essential element, but at high concentrations, it is toxic for living organisms. The present study investigated the responses of goldfish, Carassius auratus, to 96 h exposure to 30, 300, or 700 μg L−1 of copper II chloride (Cu2+). The content of protein carbonyls was higher in kidney (by 158%) after exposure to 700 mg L−1 copper, whereas in gills, liver, and brain, we observed lower content of protein carbonyls after exposure to copper compared with control values. Exposure to copper resulted in increased levels of lipid peroxides in gills (76%) and liver (95–110%) after exposure to 300 and 700 μg L−1 Cu2+. Low molecular mass thiols were depleted by 23–40% in liver and by 29–67% in kidney in response to copper treatment and can be used as biomarkers toxicity of copper. The activities of primary antioxidant enzymes, superoxide dismutase and catalase, were increased in liver as a result of Cu2+ exposure, whereas in kidney catalase activity was decreased. The activities of glutathione-related enzymes, glutathione peroxidase, glutathione-S-transferase, and glutathione reductase were decreased as a result of copper exposure, but glutathione reductase activity increased by 25–40% in liver. Taken together, these data show that exposure of fish to Cu2+ ions results in the development of low/high intensity oxidative stress reflected in enhanced activities of antioxidant and associated enzymes in different goldfish tissues.

The effects of 96 h exposure to 7.14, 35.7, or 71.4 mg L−1 of Sencor were studied on liver and plasma parameters in goldfish, Carassius auratus L. Goldfish exposure to 71.4 mg L−1 of Sencor for 96 h resulted in a decrease in glucose concentrations in plasma and liver by 55%, but did not affect liver glycogen levels. An increase in the activity of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase (by 24–27%, 32–72%, and 87–102%, respectively) occurred in plasma of Sencor exposed goldfish, whereas in liver activities of these enzymes decreased (by 15–17%, 19%, and 20%, respectively). Lactate concentration in plasma increased by 22–36% in all treated fish groups, whereas in liver it increased by 64% only after exposure to 35.7 mg L−1 of Sencor. Herbicide exposure enhanced lipid peroxide levels by 49–75% and decreased activities of catalase by 46%, glutathione reductase by 25–48% and glutathione peroxidase by 21–26% suggesting development of oxidative stress in liver. The treatment induced various histological changes in goldfish liver, such as dilated sinusoids, hypertrophy and dystrophy of hepatic cells and detachment of endothelial cytoplasm with diffuse hemorrhage. The data collectively let us propose that mild oxidative stress might be responsible for the hepatotoxicity of Sencor.

After 96 h goldfish exposure to 10, 25 or 50 mg/L of Ni(2+) no Ni accumulation was found in the brain, but lipid peroxide concentration was by 44% elevated in the brain, whereas carbonyl protein content was by 45-45% decreased in the heart. High molecular mass thiol concentration was enhanced by 30% in the heart, while in the brain low molecular mass thiol concentration increased by 28-88%. Superoxide dismutase activity was by 27% and 35% increased in the brain and heart, respectively. Glutathione peroxidase activity was lowered to 38% and 62% of control values in both tissues, whereas catalase activity was increased in the heart by 15-45%, accompanied by 18-29% decreased glutathione reductase activity. The disturbances of free radical processes in the brain and heart might result from Ni-induced injuries to other organs with more prominent changes in the heart, because of close contact of this organ with blood, whereas the blood-brain barrier seems to protect the brain.

This study aims to assess effects of 96 h goldfish exposure to 1, 10 and 100 mg/L of the herbicide, 2,4-dichlorophenoxyacetic acid (2,4-D), on metabolic indices and free radical process markers in white muscle of a commercial fish, the goldfish Carassius auratus L. Most oxidative stress markers and antioxidant enzymes were not affected at 2,4-D fish treatment. 2,4-D fish exposure induced the elevated levels of total (by 46% and 40%) and reduced (by 77% and 73%) glutathione in muscles of goldfish of 10 mg/L 2,4-D and recovery (after 100 mg/L of 2,4-D exposure) groups, respectively. However, in muscles of 100 mg/L 2,4-D exposed goldfish these parameters were depleted (by 47% and 64%). None of investigated parameters of protein and carbohydrate metabolisms changed in white muscles of 2,4-D exposed fish, with exception of lactate dehydrogenase activity, which was slightly (by 11-15%) elevated in muscles of goldfish exposed to 10-100 mg/L of 2,4-D, but also recovered. Thus, the short term exposure of goldfish to the selected concentrations of 2,4-D does not substantially affect their white muscle, suggesting the absence of any effect under the environmentally relevant concentrations.

Intensive use of pesticides, particularly dithiocarbamates, in agriculture often leads to contamination of freshwater ecosystems. To our knowledge, the mechanisms of toxicity to fish by the carbamate fungicide Tattoo that contains mancozeb [ethylenebis(dithiocarbamate)] have not been studied. The present study aimed to evaluate the effects of Tattoo on goldfish gills and blood, tissues that would have close early contact with the pollutant. Exposure of goldfish Carassius auratus to 3, 5 or 10mgL(-1) of Tattoo for 96h resulted in moderate lymphopenia (by 8 percent) with a concomitant increase in both stab (by 66-88 percent) and segmented (by 166 percent) neutrophils. An increase in the content of protein carbonyl groups in blood (by 137-184 percent) together with decreased levels of protein thiols (by 23 percent) and an enhancement of lipid peroxide concentrations (by 29 percent) in gills after exposure to 10mgL(-1) of Tattoo demonstrated the induction of mild oxidative stress in response to Tattoo exposure. At the same time, the activities of selected antioxidant enzymes were enhanced in gills: superoxide dismutase by 18-25 percent and catalase by 27 percent. A 34 percent increment in low molecular mass thiol concentrations (mainly represented by glutathione) also occurred in gills and could be related to increased activity (by 13-30 percent) of glucose-6-phosphate dehydrogenase. The results indicate that Tattoo exposure perturbs free radical processes, i.e. induces mild oxidative stress and enhances the activity of certain antioxidant and associated enzymes in goldfish gills. It is clear that goldfish respond to the presence of waterborne pesticide by adjusting antioxidant defenses through upregulation of activities of antioxidant and associated enzymes.

Metribuzin belongs to the family of asymmetrical triazine compounds and is an active ingredient in many commercial herbicides including Sencor. Effects on goldfish (Carassius auratus L.) of exposure for 96h to 7.14, 35.7 or 71.4mgL(-1) Sencor 70 WG (corresponding to 5, 25 and 50mgL(-1) of metribuzin) were examined by evaluating oxidative stress markers and activities of antioxidant and associated enzymes in gills. Fish exposed to the lowest Sencor concentration (7.14mgL(-1)) showed a 94% increase in levels of protein carbonyls in gills as well as 45% and 144% increases in the activities of glutathione peroxidase and glutathione-S-transferase. Exposure to the highest Sencor concentration (71.4mgL(-1)) resulted in reduced levels of protein carbonyls by 56% and lipid peroxides by 40%, as compared with controls, but enhanced levels of low and high molecular mass thiols by 71% and 36%, respectively. The activities of superoxide dismutase, glutathione peroxidase and glutathione-S-transferase were increased in gills of goldfish exposed to 71.4mgL(-1) Sencor. At any concentration tested, Sencor did not affect the activities of glutathione reductase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase or acetylcholine esterase in gills. The results of this study indicate that acute exposure of goldfish to Sencor had effect on free radical processes in gills and glutathione-dependent antioxidants effectively protect proteins and lipids from oxidation.

The toxicity of nickel to mammals is well studied, whereas information on nickel effects on fish is scant. Goldfish exposure to 10–50 mg L −1 of waterborne Ni 2+ for 96 h showed reduced glycogen levels by 27–33% and 37–40% in liver and white muscle, respectively, accompanied by substantial increases in blood glucose levels (by 15–99%). However, indices of oxidative damage to proteins (carbonyl proteins) and lipids (lipid peroxides) were largely unaffected by nickel exposure. In liver, the activities of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPx), were not affected by Ni 2+ treatment, while catalase activity was elevated by 26%. In white muscle, however, substantial increases in SOD (by 38–147%) and GPx (by 2.5–5.5-fold) activities appeared to compensate for decreased catalase activity (by 59–69%) in order to resist Ni-induced oxidative perturbations. Both hepatic and muscular glutathione reductase activities were suppressed by 10–30% and 12–21%, respectively, after goldfish exposure to all Ni 2+ concentrations used. However, the activity of glucose-6-phosphate dehydrogenase was remarkably enhanced (by 1.6–5.4-fold) in white muscle of Ni-exposed fish, indicating a strong potential increase in NADPH production under Ni exposure. Thus, the exposure of goldfish to 10–50 mg L −1 of Ni 2+ for 96 h induces glycogenolysis and hyperglycemia, showing some similarities with a hypoxia response, and leads to a substantial activation of defense systems against reactive oxygen species in liver and white muscle in tissue-specific and concentration-dependent manner.

Cobalt ions can enhance the generation of reactive oxygen species (ROS), which may be the reason for cobalt toxicity. This study aimed to determine whether Co(2+) toxicity in goldfish is related to induced oxidative stress in gills, heart and spleen, and to assess responses of antioxidant systems. Exposure of goldfish to 50, 100 and 150 mg L(-1) of Co(2+) for 96 h elevated total hemoglobin in blood by 23, 44 and 78%, respectively. In gills, cobalt exposure enhanced lipid peroxide levels and activities of primary antioxidant enzymes; superoxide dismutase (SOD) rose by 125% and glutathione peroxidase (GPx) increased by 53-296%. Glutathione-S-transferase (GST) activity also increased by 117-157% and glucose-6-phosphate dehydrogenase (G6PDH) enhanced by 46-96%. Heart showed limited effects of fish exposure to 50 or 100 mg L(-1) of Co(2+), but the exposure to 150 mg L(-1) of Co(2+) elevated concentrations of lipid peroxides by 123% and activities of GPx by 98% and SOD by 208%. The most substantial effects of goldfish exposure to Co(2+) were observed in spleen: a decrease in total protein concentration by 44-60% and high molecular mass thiols by 59-82%, reduced activities of catalase by 24-58% and GR by 25-68%, whereas the level of low molecular mass thiols increased by 153-279% and activities of GPx, GST, G6PDH were enhanced by 114-120%, 192-769%, and 256-581%, respectively. The data show that fish exposure to 50-150 mg L(-1) of Co(2+) elevates blood hemoglobin level, mimicking effects of hypoxia, and causes the activation of defense systems against ROS.

Cobalt is an essential element, but at high concentrations it is toxic. In addition to its well-known function as an integral part of cobalamin (vitamin B₁₂), cobalt has recently been shown to be a mimetic of hypoxia and a stimulator of the production of reactive oxygen species. The present study investigated the responses of goldfish, Carassius auratus, to 96 h exposure to 50, 100 or 150 mg L⁻¹ Co²⁺ in aquarium water (administered as CoCl₂). The concentrations of cobalt in aquaria did not change during fish exposure. Exposure to cobalt resulted in increased levels of lipid peroxides in brain (a 111% increase after exposure to 150 mg L⁻¹ Co²⁺) and liver (30-66% increases after exposure to 50-150 mg L⁻¹ Co²⁺), whereas the content of protein carbonyls rose only in kidney (by 112%) after exposure to 150 mg L⁻¹ cobalt. Low molecular mass thiols were depleted by 24-41% in brain in response to cobalt treatment. The activities of primary antioxidant enzymes, superoxide dismutase (SOD) and catalase, were substantially suppressed in brain and liver as a result of Co²⁺ exposure, whereas in kidney catalase activity was unchanged and SOD activity increased. The activities of glutathione-related enzymes, glutathione peroxidase and glutathione-S-transferase, did not change as a result of cobalt exposure, but glutathione reductase activity increased by ∼40% and ∼70% in brain and kidney, respectively. Taken together, these data show that exposure of fish to Co²⁺ ions results in the development of oxidative stress and the activation of defense systems in different goldfish tissues.

AMP-deaminase was partially purified from white skeletal muscle of goldfish, Carassius auratus. The enzyme was highly stable, showing virtually no change in activity at 1 month following the purification process when stored in 1 M KCl at 2–4°C. The specific activity of the purified enzyme was 130–150 U/mg protein, with a pH optimum of about pH 6.5. AMP-aminohydrolase (AMPD) showed non-Michaelis–Menten kinetics, with a S0.5 (half saturation by the substrate) for AMP of 0.73 ± 0.03 mM, a Hill coefficient of 2.01 ± 0.26, and a V max (maximum velocity) of 176 ± 46 U/mg protein. Both sodium and potassium ions activated goldfish AMPD at low concentrations, with maximal activation at about 80 mM of each chloride salt, whereas higher concentrations became inhibitory. Magnesium and calcium ions also inhibited goldfish muscle AMPD, as did phosphate and fluoride; at a concentration of 8 mM, each anion reduced activity by about 66%. ADP and ATP were strong activators and both demonstrated concentration-dependent activation, with maximal effects at 0.5–1.5 mM. Fish exposure to a high concentration of oxygen (18–20 mg/l against 5–6 mg/l in the control) and recovery to the initial level induced a redistribution of AMPD between free and bound forms in goldfish white muscle and brain in a tissue-dependent manner. A spatial–temporal redistribution may be among the mechanisms regulating enzyme operation in vivo. Possible regulatory mechanisms of AMP-deaminase function in fish muscle are discussed.

AMP-deaminase was purified to electrophoretic homogeneity from white skeletal muscle of a teleost fish, the common carp, Cyprinus carpio. The purified enzyme was highly stable and showed non-Michaelis-Menten kinetics with a S(0.5) value for AMP of 2.52+/-0.16 mM (SEM) and a Hill coefficient of 1.19+/-0.11. Specific activity of the purified enzyme was 1000-1200 U/mg protein. The pH optimum was 6.3 and the enzyme was activated by ADP and ATP, but inhibited by phosphate and fluoride. Low concentrations of NaCl and KCl (100-150 mM) activated, whereas higher concentrations were inhibitory. Free radicals inactivated the enzyme, decreasing V(max) by one-half but not affecting S(0.5) or Hill coefficient. Possible regulatory mechanisms of AMP-deaminase activity in fish muscle are discussed.

The purpose of this paper is to provide a brief review of the current knowledgeregarding metabolism and toxicity of copper and copper-based pesticides in living organisms.Copper is an essential trace element in all living organisms (bacteria, fungi, plants, and animals),because it participates in different metabolic processes and maintain functions of organisms. Thetransport and metabolism of copper in living organisms is currently the subject of many studies.Copper is absorbed, transported, distributed, stored, and excreted in the body via the complex ofhomeostatic processes, which provide organisms with a needed constant level of this micronutrientand avoid excessive amounts. Many aspects of copper homeostasis were studied at the molecularlevel. Copper based-pesticides, in particularly fungicides, bacteriocides and herbicides, are widelyused in agricultural practice throughout the world. Copper is an integral part of antioxidantenzymes, particularly copper-zinc superoxide dismutase (Cu,Zn-SOD), and plays prominent rolesin iron homeostasis. On the other hand, excess of copper in organism has deleterious effect,because it stimulates free radical production in the cell, induces lipid peroxidation, and disturbsthe total antioxidant capacity of the body. The mechanisms of copper toxicity are discussed in thisreview also.

Molecular mechanisms of toxicity by the metribuzin-containing herbicide Sencor to living organisms, particularly fish, have not yet been extensively investigated. In the present work, we studied the effects of 96 h exposure to 7.14, 35.7, or 71.4 mg L(-1) of Sencor (corresponding to 5, 25, or 50 mg L(-1) of its herbicidal component metribuzin) on goldfish (Carassius auratus L.), examining the histology, levels of oxidative stress markers, and activities of antioxidant and related enzymes in kidney as well as hematological parameters and leukocyte profiles in blood. The treatment induced various histopathological changes in goldfish kidney, such as hypertrophy of intertubular hematopoietic tissue, small and multiple hemorrhages, glomerular shrinkage, a decrease in space between glomerulus and Bowman's capsule, degeneration and necrosis of the tubular epithelium. Sencor exposure also decreased activities of selected enzymes in kidney; activities of catalase decreased by 31-34%, glutathione peroxidase by 14-33%, glutathione reductase by 17-25%, and acetylcholinesterase by 31%. However, glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities increased by 25-30% and 22% in kidney after treatment with 7.14 or 35.7 mg L(-1) and 71.4 mg L(-1) Sencor, respectively. Kidney levels of protein carbonyls increased by 177% after exposure to 35.7 mg L(-1) of Sencor indicating extensive damage to proteins. Lipid peroxide concentrations also increased by 25% after exposure to 7.14 mg L(-1) of Sencor, but levels were reduced by 42% in the 71.4 mg L(-1) exposure group. The data indicate that induction of oxidative stress is one of the mechanisms responsible for Sencor toxicity to fish.

After 96 h goldfish exposure to 10, 25 or 50 mg/L of Ni(2+) no Ni accumulation was found in the brain, but lipid peroxide concentration was by 44% elevated in the brain, whereas carbonyl protein content was by 45-45% decreased in the heart. High molecular mass thiol concentration was enhanced by 30% in the heart, while in the brain low molecular mass thiol concentration increased by 28-88%. Superoxide dismutase activity was by 27% and 35% increased in the brain and heart, respectively. Glutathione peroxidase activity was lowered to 38% and 62% of control values in both tissues, whereas catalase activity was increased in the heart by 15-45%, accompanied by 18-29% decreased glutathione reductase activity. The disturbances of free radical processes in the brain and heart might result from Ni-induced injuries to other organs with more prominent changes in the heart, because of close contact of this organ with blood, whereas the blood-brain barrier seems to protect the brain.

This study investigated the effects of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) on free radical-related processes in tissues of goldfish given 96 h exposures to 1, 10 or 100 mg/L of 2,4-D as well as 96 h recovery from the 100 mg/L treatment. In liver, 2,4-D exposure increased levels of protein carbonyls and lipid peroxides by 36-53% and 24-43%, respectively, but both parameters reverted during recovery, whereas in brain glutathione status improved in response to 2,4-D. Lipid peroxide content in kidney was enhanced by 40-43% after exposure to 2,4-D with a decrease during recovery. Exposure to 2,4-D also reduced liver acetylcholinesterase activity by 31-41%. The treatment increased catalase activity in brain, but returned it to initial levels after recovery. In kidney, exposure to 100 mg/L of 2,4-D caused a 33% decrease of superoxide dismutase activity. Thus, goldfish exposure to 2,4-D induced moderate oxidative stress in liver and kidney and mild oxidative stress in brain.

Fish gills are target organs for waterborne metal ions and this work aimed to investigate the effects of waterborne Ni(2+) (10, 25 and 50 mg L(-1)) on goldfish gills. A special focus was on the relationship between Ni uptake and the homeostasis of reactive oxygen species (ROS) in the gills, the tissue, in direct contact with the metal pollutant. Ni-accumulation in the gills occurred as a function of exposure concentration (R(2)=0.98). The main indices of oxidative stress, namely carbonyl proteins (CP) and lipid peroxides (LOOH), decreased by 21-33% and 21-24%, as well as the activities of principal antioxidant enzymes superoxide dismutase and glutathione-dependent peroxidase, by 29-47% and 41-46%, respectively, in gills of Ni-exposed fish. One of the main players in the antioxidant defense of gills seems to be catalase, which increased by 23-53% in Ni-treated fish, and low molecular mass thiol-containing compounds (L-SH), exceeding untreated controls by 73-105% after fish exposure to 10-50 mg L(-1) of Ni(2+). The increased level of L-SH, mainly represented by reduced glutathione, was supported by enhanced activities of glutathione reductase (by 27-38%), glutathione-S-transferase (56-141%) and glucose-6-phosphate dehydrogenase (by 96-117%) and demonstrates the ability of the antioxidant system of gills to resist Ni-induced oxidative stress.

Tattoo belongs to the group of carbamate fungicides and contains Mancozeb (ethylene(bis)dithiocarbamate) as its main constituent. The toxicity of Mancozeb to living organisms, particularly fish, is not resolved. This work investigated the effects of 96 h of exposure to 3, 5, or 10 mg L−1 of Tattoo (corresponding to 0.9, 1.5, or 3 mg L−1 of Mancozeb) on the levels of oxidative stress markers and the antioxidant enzyme system of brain, liver, and kidney of goldfish, Carassius auratus). In liver, Tattoo exposure resulted in increased activities of superoxide dismutase (SOD) by 70%–79%, catalase by 23%–52% and glutathione peroxidase (GPx) by 49%. The content of protein carbonyls (CP) in liver was also enhanced by 92%–125% indicating extensive damage to proteins. Similar increases in CP levels (by 98%–111%) accompanied by reduced glucose-6-phosphate dehydrogenase activity (by 13%–15%) was observed in kidney of fish exposed to Tattoo; however, SOD activity increased by 37% in this tissue after treatment with 10 mg L−1 Tattoo. In brain, a rise in lipid peroxide level (by 29%) took place after exposure to 10 mg L−1 Tattoo and was accompanied by elevation of high-molecular mass thiols (by 14%). Tattoo exposure also resulted in a concentration-dependent decrease in glutathione reductase activity (by 26%–37%) in brain. The data collectively show that exposure of goldfish to 3–10 mg L−1 of the carbamate fungicide Tattoo resulted in the development of mild oxidative stress and activation of antioxidant defense systems in goldfish tissues. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1227–1235, 2014.

Toxic and carcinogenic effects of nickel compounds are suggested to result from nickel-mediated oxidative damage to macromolecules and/or inhibition of cellular antioxidant defenses. We investigated the effects of waterborne Ni(2+) (10, 25 and 50 mg/L) on the blood and blood-producing tissues (kidney and spleen) of goldfish to identify relationships between Ni accumulation and oxidative stress. Whereas the main hematological parameters (total hemoglobin and hematocrit) were unaffected, Ni(2+) exposure had substantial influence on goldfish immune system, causing lymphopenia. Ni accumulation increased renal iron content (by 49-78%) and resulted in elevated lipid peroxide (by 29%) and protein carbonyl content (by 274-278%), accompanied by suppression of the activities of superoxide dismutase (by 50-53%), glutathione peroxidase (15-45%), glutathione reductase (31-37%) and glucose-6-phosphate dehydrogenase (20-44%), indicating development of oxidative stress in kidney. In contrast to kidney, in spleen the activation of glutathione peroxidase (by 34-118%), glutathione-S-transferase (by 41-216%) and glutathione reductase (by 47%), as well as constant levels of low molecular mass thiols and metals together with enhanced activity of glucose-6-phosphate dehydrogenase (by 41-94%) speaks for a powerful antioxidant potential that counteracts Ni-induced ROS production. Further, as Ni accumulation in this organ was negligible, Ni-toxicity in spleen may be minimized by efficient exclusion of this otherwise toxic metal.