Ameliorative effect of lycopene on antioxidant status in Cyprinus carpio during pyrethroid deltamethrin exposure

The aim of the present study was to investigate the ameliorative properties of lycopene against the toxic effects of deltamethrin (DM) by examining oxidative damage markers such as lipid peroxidation and the antioxidant defense system components in carp (Cyprinus carpio). The fish were divided into seven groups of 15 fish each and received the following treatments: Group 1, no treatment; Group 2, orally administered corn oil; Group 3, oral lycopene (10 mg/kg body weight); Group 4, exposure to 0.018 μg/L DM; Group 5, exposure to 0.018 μg/L DM plus oral administration of 10 mg/kg lycopene; Group 6, exposure to 0.036 μg/L DM; and Group 7, exposure to 0.036 μg/L DM plus oral administration of 10 mg/kg lycopene. Treatment was continued for 14 days, and at the end of this period, blood and tissue (liver, kidney, and gill) samples were collected. Levels of malondialdehyde (MDA) and reduced glutathione (GSH) as well as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were determined in blood and tissues for measurement of oxidant-antioxidant status. A significant elevation in the level of MDA, as an index of lipid peroxidation, and reductions in antioxidant enzyme activities (SOD, CAT, and GSH-Px) and low molecular weight antioxidant (GSH) levels were observed in DM-exposed fish. Treatment with lycopene attenuated the DM-induced oxidative stress by significantly decreasing the levels of MDA. In addition, lycopene significantly increased the SOD, CAT, and GSH-Px activities and the level of GSH. The present results suggest that administration of lycopene might alleviate DM-induced oxidative stress.     

Selenium and vitamin E, natural antioxidants, protect rat cerebral cortex against dimethoate-induced neurotoxicity

Pesticides have been used in agriculture to enhance food production by eradicating unwanted insects and controlling disease vectors, nevertheless occupational exposure to high levels of these compounds can lead to neurodegenerative disorders, characterized by serious oxidative and neurotoxic effects. However, there is a lack of consensus as to which determinations are best used to quantify future risks arising from xenobiotic exposure and natural antioxidant interventions. Our study aims to determine the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress in cerebral cortex tissue induced by dimethoate, an organophosphorus pesticide. Adult Wistar rats were exposed either to dimethoate (0.2 g/L of drinking water), dimethoate + selenium (0.5 mg/kg of diet), dimethoate + vitamin E (100 mg/kg of diet), or dimethoate + selenium + vitamin E, for 30 days. Exposure to dimethoate increased malondialdehyde levels, protein carbonyl groups and advanced oxidation protein products, while Na⁺K⁺-ATPase, acetylcholinesterase and butyrylcholinesterase activities decreased in the cerebral cortex. An increase in glutathione peroxidase, superoxide dismutase and catalase activities and a decrease in glutathione, non-protein thiols and vitamin C levels were observed. Administration of selenium and/or vitamin E through the diet in dimethoate treated rats ameliorated the biochemical parameters cited above. The histological findings confirmed the biochemical results. The model of this study that we employed characterized the relationships between dimethoate-induced neurotoxicity and its alleviation by natural antioxidants like selenium and vitamin E. These elements may be considered beneficial for the protection of cerebral cortex against injury induced by dimethoate.     

Modulation of ethion-induced hepatotoxicity and oxidative stress by vitamin E supplementation in male Wistar rats

Organophosphorus insecticides (OPIs) may induce oxidative stress leading to generation of free radicals and alteration in antioxidant system of animals. Many studies reported that enzymatic and non-enzymatic antioxidant may play protective role against OPIs induced toxicity in human and rats. The aim of present study was to investigate the possible protective role of vitamin E on ethion-induced hepatotoxicity in rats using qualitative, quantitative and biochemical approaches. Adult male albino rats of Wistar strain were randomly divided into four groups; each group consists of six animals. Animals were treated for a period of 28 days. Group I (control group received corn oil); Group II [ethion treated (2.7 mg/kg bw/day)]; Group III (vitamin E treated (50 mg/kg of bw/day)]; Group IV (ethion + vitamin E treated). Animals were sacrificed after 7, 14, 21 and 28 days by decapitation and liver tissue was used for the measurement of proteins, lipid peroxidation (LPO), reduced glutathione (GSH) content and activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) glutathione reductase (GR) and glutathione-S-transferase (GST). Erythrocytes were analyzed for acetyl cholinesterase activity. The result of this study shows that in vivo administration of ethion caused a significant induction of oxidative damage in liver tissue as evidenced by increased level of LPO and decreased GSH content. Ethion toxicity also led to a significant increase in the activities of SOD, CAT, GPx and GST in liver tissue. In addition, decrease in GR activity was observed in ethion administered rats compared to control. Histopathological findings revealed that exposure to ethion caused damage in liver tissue. However, simultaneous supplementation with vitamin E restored these parameters partially. In conclusion, the results of the current study revealed that ethion-induced toxicity caused lipid peroxidation, alterations in the antioxidant enzymes and histopathological changes in liver. Supplementation of vitamin E exhibited protective effect by inhibiting ethion-induced toxicity in liver and erythrocytes.     

Protective effect of vitamin C against chlorpyrifos oxidative stress in male mice

Pesticides may induce oxidative stress leading to generate free radicals and alternate antioxidant or oxygen free radical scavenging enzyme system. This study was conducted to investigate the acute toxicity of chlorpyrifos toward male mice and the oxidative stress of the sub-lethal dose (1/10 LD₅₀) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-S-transferase (GST) activities. Also, the protective effects of vitamin C (200 mg/kg body weight, bw) 30 min before or after administration of chlorpyrifos were investigated. The results demonstrated that the LD₅₀ value of chlorpyrifos was 134.95 mg/kg bw. The oral administration of 13.495 mg/kg chlorpyrifos significantly caused elevation in LPO level and the activities of antioxidant enzymes including CAT, SOD and GST. However, GPx activity remained unchanged, while the level of GSH and G6PD activity were decreased. Vitamin C treatment to chlorpyrifos intoxicated mice decreased LPO level and GST activity, normalized CAT, SOD and G6PD activities, while GSH content was increased. We conclude that vitamin C significantly reduces chlorpyrifos-induced oxidative stress in mice liver and the protective effect of the pre-treatment with vitamin C is better than the post-treatment.     

Dimethoate induced biochemical perturbations in rat pancreas and its attenuation by cashew nut skin extract

The significant antiradical activity of cashew skin extract was previously described. In this investigation, the extent of protection offered by cashew nut skin extract (CSE) against the damage induced in rat pancreas by sub chronic doses dimethoate (DM), an organophosphorous pesticide was studied. Rats were supplemented with CSE at 20 mg/kg b.w./d after a daily dose of DM at 40 mg/kg/d b.w. for 2 months. Weekly random blood glucose, oral glucose tolerance test (OGTT); pancreatic damage markers like amylase and lipase; oxidative damage markers such as reactive oxygen species generated, extent of lipid peroxidation, host antioxidant defenses like reduced glutathione (GSH); GSH-dependent enzyme activities viz., glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR); free radical scavenger enzymes viz., catalase and superoxide dismutase (SOD); xenobiotic metabolizing enzymes like DT-diaphorase and NADPH-diaphorase were measured in the four different groups namely (1) control, (2) DM treated, (3) CSE supplemented, (4) CSE supplements following DM treatment. Random blood glucose levels increased significantly on exposure to DM compared to that in control rats (119 ± 5 mg/dl vs. 92 ± 4 mg/dl), while the blood glucose levels in CSE supplemented rats were comparable to that of controls. DM treated rats exhibited impaired glucose tolerance at the end of two months as indicated by OGTT, while DM treated rats with CSE supplements showed normal glucose tolerance. Pancreatic specific marker enzymes like amylase and lipase in serum were restored to normalcy in rats supplemented with CSE following treatment with DM which otherwise was increased in the DM treated rats. Distinctly lower levels of GSH, increased levels of ROS, higher extent of lipid peroxidation, along with alterations in antioxidant enzymes and increase in xenobiotic metabolizing enzymes were evident in pancreas of DM treated rats. However, CSE supplement ameliorated the biochemical alterations in the pancreatic milieu in DM treated rats. Treatment with CSE significantly protected rat pancreas from injury, thus ameliorating and restoring tissue antioxidant status and also conferring normal glucose tolerance. The active components present in cashew skin extract can perhaps be effective in reducing the extent of pancreatic injury and in overcoming tissue damage caused by exposure to dimethoate.     

Amelioratory effect of vitamin E on organophosphorus insecticide diazinon-induced oxidative stress in mice liver

Considering that the involvement of reactive oxygen species (ROS) has been implicated in the toxicity of organophosphate insecticides (OPIs), the aim of this study was to investigate the ameliorative properties of vitamin E (vitE) against the subchronic effect of diazinon (DZN) on oxidative damage markers such as lipid peroxidation (LPO) and the antioxidant defense system (ADS) in the liver of male MFI albino mice. The groups were intraperitoneally (i.p) administered with either vehicle or vitE (100 mg/kg body weight) or ¼ LD₅₀ of DZN (16.25 mg/kg b.w.) or ½ LD₅₀ of DZN; 32.5 mg/kg b.w) or ¼ LD₅₀-DZN + vitE or ½ LD₅₀ + vitE every consecutive day for 14 days. Hepatic damage markers analysis revealed that alanine transferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were significantly decreased in both DZN doses. Also, the significantly increased levels of biomarkers of oxidative stress as LPO and protein carbonyl (PC) and the decreased antioxidant defenses like reduced glutathione (GSH), and free radical scavenger enzymes viz., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GSH-Rx) were noted in DZN-treated groups as compared to control group. Distinctly lower levels of GSH and increased levels of LPO, along with alterations in endogenous antioxidant enzymes were evident in hepatic toxicity of DZN which is dose-dependent. Hepatic specific marker enzymes were restored to normalcy in mice supplemented with vitE following treatment with DZN which otherwise was decreased in the DZN-treated mice. The results show that co-treatment of vitE with DZN prevents or diminishes the oxidative stress of DZN-treated mice and may act as a putative protective agent against DZN-induced liver tissue injury.     

The effects of Saw palmetto on flumethrin-induced lipid peroxidation in rats

In the present study, 40 male Wistar albino rats were used and divided into 4 groups. The first group served as the control group; the second group was administered Saw palmetto extract at the dose of 20 mg/kg/bw; the third group was administered flumethrin at the dose of 15 mg/kg/bw; and the fourth group was administered a combination of 20 mg/kg/bw Saw palmetto extract and 15 mg/kg/bw flumethrin, for 21 days, orally. After the trial period, blood and tissue (liver, kidney and brain) samples were taken from the rats. Saw palmetto extract did not cause significant alterations in plasma and tissue malondialdehyde (MDA) levels, serum and tissue nitric oxide (NO) levels, erythrocyte and tissue superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities when compared to the controls (p > 0.05). Flumethrin led to increased plasma and tissue MDA levels, serum and tissue NO levels, tissue GSH-Px activities and decreased erythrocyte and tissue SOD and CAT activities, and erythrocyte GSH-Px activity, compared to the controls (p < 0.05). The flumethrin and Saw palmetto extract combination increased erythrocyte SOD activity and decreased brain GSH-Px activity as compared to flumethrin (p < 0.05). In conclusion, it was determined that Saw palmetto extract did not cause any negative effect on the prooxidant-antioxidant balance. While flumethrin stimulated lipid peroxidation; Saw palmetto extract at the dose of 20 mg/kg/bw did not exhibit enough antioxidant effect in rats.     

Protective effects of Nigella sativa oil on propoxur-induced toxicity and oxidative stress in rat brain regions

Propoxur (PPr) is a widely used broad spectrum carbamate insecticide mainly used to control household pests. Because of the widespread use of pesticides for domestic and industrial applications, evaluation of their neurotoxic effects is of major concern to public health. The aim of the present study was to evaluate the possible protective effects of Nigella sativa oil (NSO), an antioxidant agent, against PPr-induced toxicity and oxidative stress in different brain regions of rats including cerebellum, cortex and hippocampus. In the present study, 32 male Sprague-Dawley rats were used and divided into four equal groups. Group 1 was allocated as the control group. Groups 2-4 were orally administered 1 ml/kg/bw/day NSO, 8.51 mg/kg/bw/day PPr or NSO plus PPr, respectively, for 30 days. Lipid peroxidation (LPO), protein carbonyl content (PCC) and acetylcholine esterase activity (AChE) were determined. Enzymatic antioxidant activities [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST)] and non-enzymatic antioxidants [reduced glutathione (GSH)] were determined. PPr treatment significantly increased the levels of LPO, PCC and oxidized glutathione (GSSG) in brain regions. On the contrary, levels of GSH and the activities of SOD, CAT, GSH-Px, GST and AChE were significantly decreased. NSO treatment to PPr intoxicated rats restored such biochemical parameters to within control levels except GST activity, emphasizing its antioxidant role. We conclude that NSO significantly reduces PPr-induced toxicity and oxidative stress in rat brain regions via a free radicals scavenging mechanism.     

Effect of α tocopherol and selenium on antioxidant status, lipid peroxidation and hepatopathy induced by malathion in chicks

The objective of the present study was to investigate the role of α tocopherol and selenium on malathion induced hepatic damage, and antioxidant defense in chicks. The chicks were divided into three groups. First group received malathion 10 mg/kg BW, orally for 60 days, the second group received the same dose of malathion but was supplemented with α tocopherol and selenium for 60 days and the third group served as the control. A compromised antioxidant capacity as evidenced by increased levels of erythrocytic lipid peroxidation and decreased concentration of vitamin E and decreased activity of glutathione peroxidase was observed in chicks following the administration of malathion. An improved antioxidant status was observed in chicks of second group with α tocopherol and selenium supplementation including higher concentration of vitamin E, increased activity of glutathione peroxidase and lower levels of lipid peroxidation. Histopathological studies of liver in the chicks which received malathion exhibited, moderate to severe degenerative and necrotic changes in the hepatocytes. The correlation of decreased antioxidant status of chicks with degenerative changes in liver suggests that lipid peroxidation may be one of the important mechanism in the chronic toxicity of malathion. The results indicate that α tocopherol and selenium were effective in partially alleviating degenerative changes induced by malathion in the liver of chicks by attenuating processes leading to lipid peroxidation.     

Effects of thiacloprid, deltamethrin and their combination on oxidative stress in lymphoid organs, polymorphonuclear leukocytes and plasma of rats

Deltamethrin and thiachloprid are an α-cyano class pyrethroid and neonicotinoid insecticide, respectively. Recently, a pesticide combining deltamethrin and thiacloprid has also been released. In the present study, the acute and subacute toxic effects of deltamethrin, thiachlopride, and a combination of these insecticides, on the lymphoid organs (spleen, thymus and bone marrow), polymorphonuclear leukocytes (PMNs) and plasma of rats, were determined to better understand mammalian antioxidant-oxidant and inflammatory system responses. For this purpose, rats were treated orally with different doses of thiacloprid (single acute dose of 112.5 mg/kg); subacute dose of 22.5 mg/kg/day for 30 days; deltamethrin (single acute dose of 15 mg/kg); subacute dose (3 mg/kg/day for 30 days), or a combination of these pesticides. Results were compared with those from a comparable dosing regimen with the known immunosuppressive drug cyclophosphamide. Pesticide treatments caused significant changes in the levels of liver and kidney injury markers. Antioxidant enzyme (catalase and glutathione peroxidase), glutathione and plasma antioxidant levels decreased but lipid peroxidation increased in all lymphoid organs and the plasma. Glutathione-S-transferase and especially DT-diaphorase activity, decreased after thiacloprid treatment. Myeloperoxidase activity, carbonyl content, lipid peroxidation and total nitrite levels increased in PMNs and plasma. When evaluated as a whole, the oxidative and inflammatory stresses seen in the pesticide combination groups were not much more pronounced than in the groups treated with a single pesticide. In terms of the evaluated biochemical parameters, the pesticides showed similar effects to cyclophosphamide.     

Changes in selected immunological parameters and antioxidant status of rainbow trout exposed to malachite green (Oncorhynchus mykiss, Walbaum, 1792)

In this study, the effects of malachite green on selected immunological parameters, oxidative stress and antioxidant status biomarkers in blood, liver, kidney, spleen and gill of rainbow trout, Oncorhynchus mykiss, was examined. During 5 days the malachite green was applied at concentrations of 1/15,000 and 1/150,000 for 30 s and 60 min, respectively. Immunological parameters (nitroblue tetrazolium (NBT) activity, total plasma protein (TP), total immunoglobulin (TI)) and biochemical parameters (lipid peroxidation (MDA), catalase (CAT) activity, reduced glutathione (GSH) levels) were evaluated after exposed to malachite green. It has been observed that NBT activity (p < 0.05, p < 0.001), total protein (p < 0.01, p < 0.001) and total immunoglobulin (p < 0.05, p < 0.001) levels were decreased compared with control group. In the rainbow tout exposed to malachite green duration 5 days significantly increased lipid peroxidation, which might be associated to decreased levels of reduced glutathione and catalase activity in the whole tissues of O. mykiss (p < 0.05, p < 0.01, p < 0.001 for each cases).     

Subacute oral toxicity of chlorpyriphos and protective effect of green tea extract

This paper reports the effect of green tea administration following subacute toxicity caused by exposure to organophosphorus pesticide chlorpyriphos in liver of rats. Four groups containing five male Sprague-Dawley rats each were selected. Group I served as control. Group II rats were permitted free access to solubilised crude extract of green tea (1.5%w/v in water) as the sole drinking fluid. Group III rats were given a single daily oral dose of chlorpyriphos (30 mg/kg bodyweight in corn oil). Group IV rats received oral dose of pesticide and green tea extract simultaneously. All rats were sacrificed after 15 days. Significant damage to liver was observed via increased serum levels of transaminases and alkaline phosphatase. Lipid peroxidation showed a 5-fold increase in pesticide exposed rats compared to control. In contrast, levels of antioxidant GSH, glutathione-dependent enzymes like glutathione peroxidase (GPx), glutathione S-transferase (GST) and free radical scavengers like catalase (CAT) and superoxide dismutase (SOD) were significantly lower than those of the control group reinforcing oxidative damage. The use of green tea extract appeared to be beneficial to rats, although not to a great extent in significantly reducing and reversing the damage sustained by pesticide exposure and favors recovery.     

Effects of vitamin E and selenium on tissue bio-element status in organophosphate toxicity of rats

The present study was designed to investigate the effects of vitamin E (vit E), selenium (Se) and vit E + Se against organophosphate (OP) toxicity in tissues’ trace and major element levels and erythrocyte antioxidant enzyme activities of rats. Trace and major element concentrations in the tissues were measured by inductively coupled plasma-optical emission spectroscopy. Erythrocyte antioxidant enzyme activities were studied by using spectrophotometer. Antioxidant enzyme activities such as superoxide dismutase, glutathione peroxidase and catalase increased in the fenthion-treated groups (control) more than that of sham group subjects. Heart and pectoral muscle tissue Se and Zn concentrations in the control group were higher than sham group. However, jejunum, kidney, liver and pancreas Se and Zn concentrations in the control group were found to be lower than those in the sham group. The Mn concentrations in the all of the tissues were lower in the control group when compared with the sham group. Brain, heart, jejunum, kidney and pancreas Fe concentrations and heart, jejunum, liver, pectoral muscle and pancreas Cu concentrations were found to be lower in the control group. The treatment of vit E, Se and vit E + Se were increased bio-element levels in the many tissue. In conclusion, the results of the present study demonstrate that the tissue trace and major element concentrations and enzymatic antioxidant system were significantly affected OP toxicity. Furthermore, we have shown an association between bio-elements and antioxidant enzymes in OP toxicity. In addition, administration of vit E, Se and vit E + Se might regulate some trace and major element levels in the many tissues.     

Effect of ginger supplementation on developmental toxicity induced by fenitrothion insecticide and/or lead in albino rats

Evaluation of the antioxidant and antiteratogenic role of ginger Zingiber officinale polyphenols against the toxicity induced by fenitrothion and/or lead in female albino rats were investigated. Adult virgin females were divided into 8 groups and were orally treated as follow: control (C), 1% w/w of ginger (G), 120 μg/animal lead as lead acetate (L), 10 mg/kg of fenitrothion (F), lead (120 μg/animal) fenitrothion (10 mg/kg) (LF), ginger (1%w/w) + fenitrothion (10 mg/kg) (GF), ginger (1%w/w) + lead (120 μg/animal) (GL), ginger (1%w/w) + lead (120 μg/animal) + fenitrothion (10 mg/kg) (GLF). Treatments were expanded for 28 days before pregnancy and during gestation period from zero to 6th day. Blood samples were taken at the day 20th of gestation and animals were sacrificed to investigate the effect of tested substances on dams and development of their fetuses. Inhibition in AchE in (F) and (LF) groups and elevation in plasma AchE in (L) groups were observed. Elevation in oxidative stress biomarker malondialdehyde (MDA) was recorded in all intoxicated groups concomitants with reduction in total reduced glutathione (GSH) and reduction in the activity of glutathione S-transferase (GST). Elevation in liver function biomarkers alanin amintransferase (ALT) and aspartate aminotransferase (AST) and reduction in plasma total protein and albumin were recorded in (F), (L) and (LF). Supplementation with ginger in diet attenuates the alteration in MDA, GSH, GST, ALT and AST, however, it failed to counteract the effect of F, L and LF on AchE, total protein and albumin. Significant alterations in maternal toxicity were recorded in (GF, GL, LF and GLF) compared with control group. Also, parameters of embryotoxicity and fetotoxicity indicated significant decrease in litter number that observed in F and L and the number of dead fetus/dam and litters number increased in L group. Supplementation with ginger decreased each of the number of died fetus, growth retardation and fetal length, while, it increased fetal weight. As regards to, teratological aspects, the percentage of skeletal malformations and visceral anomalies were observed in all feti obtained from treated groups with different percentages. Supplementation with ginger slightly attenuates the developmental toxicity of fenitrothion and/or lead.     

Monocrotophos induced lipid peroxidation and oxidative DNA damage in rat tissues

Monocrotophos (dimethyl(E)-1-methyl-2-(methyl carbamoyl) vinyl phosphate, MCP), a substituted vinyl phosphate, is a potent systemic toxicant and used for control of variety of pests. The present study is undertaken to evaluate the genotoxic potential of monocrotophos and time-dependent repair of the damaged DNA in rats, using single cell gel electrophoresis or comet assay. The involvement of oxidative stress was also examined by estimation of thiobarbituric acid reactive substances (TBARS) in the tissues of MCP exposed rats. The rats were given oral exposure of 4.5 and 9 mg MCP/kg body weight once as well as 0.3 and 0.6 mg MCP/kg body weight for 60 days. A dose-dependent increase was recorded in the levels of TBARS in the liver, kidney, spleen and brain of MCP exposed rats. Cytotoxicity of MCP is evident from the histopathological studies of rat tissues. The level of DNA damage was estimated by scoring 50 cells per animal, dividing into five types, Types 0, I, II, III and IV. The results clearly indicated that exposure to MCP, acutely or chronically, caused a dose-dependent increase in the number of damaged nuclei of Types II, III and IV in the liver, kidney, spleen and brain of rats. When the DNA damage was studied 48 and 72 h post MCP treatment, a significant reduction in the number of types III and IV nuclei was observed in all the tissues indicating a time-dependent repair. From the present study, it can be concluded that oxidative stress may be involved in the toxicity of MCP and MCP induces DNA damage in all the rat tissues exhibiting genotoxic potential in vivo.     

Effects of N-acetylcysteine on oxidative responses in the liver of fenthion exposed Cyprinus carpio

The aim of this study was to evaluate the effects of different N-acetylcysteine doses on the tolerance to fenthion-induced oxidative stress, alterations in glutathione metabolism and cholinesterase specific activities in the liver by using freshwater fish Cyprinus carpio (Cyprinidae) as a model organism. An acute toxicity study was carried out to determine 96-h median lethal concentration of fenthion for this species (2.16 mg/L) and 80% of this concentration was applied in toxicity studies. Four groups, each containing eight fish were constituted as follows: Control group, fenthion treated group, 0.5 or 400 mg/kg NAC-injected + fenthion-treated groups. Biochemical analyses were carried out spectrophotometrically. Fenthion treatment significantly decreased total glutathione and glutathione levels, glutathione/glutathione disulfide ratio together with glutathione reductase and γ-glutamylcysteine synthetase specific enzyme activities. The higher dose of N-acetylcysteine increased the toxic effects of fenthion and γ-glutamyl transpeptidase specific activity while decreasing glutathione S-transferase specific activity. However, injection of the lower dose provided a limited protection against fenthion toxicity. In all exposure groups, lipid peroxidation increased and total protein levels decreased, while protein depletion was prevented by low dose of N-acetylcysteine application. Acetylcholinesterase and butyrylcholinesterase activities were at similar levels in the liver of C. carpio. A dose-dependent inhibition was observed in butyrylcholinesterase activity by N-acetylcysteine application. The results showed that fenthion had a significant oxidative stress inducing potential through the reduction of glutathione redox capacity. The critical point for overcoming oxidative stress by N-acetylcysteine in fenthion toxicity was the selection of the dose; N-acetylcysteine exerted its toxic effects by means of oxidative stress in fish liver at the higher dose.     

The effects of metribuzin on early life stages of common carp (Cyprinus carpio)

Metribuzin belongs to the triazine group of herbicides, which are frequently used in agriculture. The aim of this study was to assess the impact of metribuzin on growth and development of early life stages of fish. Subchronic toxic effects of metribuzin at concentrations of 0.9, 4, 14, and 32 mg/L on embryos and larvae of common carp (Cyprinus carpio) were investigated during a 30 day toxicity test under experimental conditions. Exposure to metribuzin at 32 mg/L was associated with increased mortality. Negative effects on total body length, weight, and inhibition of specific growth rate were induced by all experimental concentrations. Length and weight parameters were the most sensitive. The negative impact of metribuzin was observed in the highest tested concentration beginning on day 6 of exposure. Retardation of early ontogeny was associated with concentrations ?4 mg/L. Histological examination revealed changes in liver and caudal kidney after 30 days exposure to 32 mg/L. Based on growth parameters, development, and histological examination, the Lowest Observed Effect Concentration (LOEC) value was 0.9 mg/L.     

Oxidative parameters of Rhamdia quelen in response to commercial herbicide containing clomazone and recovery pattern

In this study, fish Rhamdia quelen, were exposed to different concentrations of herbicide clomazone: 0.0 (control), 0.45 and 0.91 mg L⁻¹. After exposure for 8 days to herbicide, fish were transferred to clean water for a recovery period (8 days). Oxidative stress indicators such as thiobarbituric acid reactive substances (TBARS) levels and protein carbonyl content, as well as antioxidant defenses, such as catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST), ascorbic acid and non-protein thiols levels were studied, using the liver, brain and muscle tissues. Herbicide exposure increased TBARS in muscle and in liver at higher concentration. In liver protein carbonylation increased and catalase activity did not change in fish exposed to herbicide. SOD enhanced in liver at concentration of 0.91 mg L⁻¹. GST, ascorbic acid and non-protein thiols levels increase at both concentrations. At the end of the recovery period the most of the parameters recovered whereas GST and ascorbic acid remain elevated. The present study demonstrates the occurrence of disorders in antioxidant parameters and importance in the assessment of the potential risk of herbicides as clomazone on fish species.