Dapsone induces oxidative stress and impairs antioxidant defenses in rat liver

Dapsone (DDS) is currently used in the treatment of leprosy, malaria and in infections with Pneumocystis jirovecii and Toxoplasma gondii in AIDS patients. Adverse effects of DDS involve methemoglobinemia and hemolysis and, to a lower extent, liver damage, though the mechanism is poorly characterized. We evaluated the effect of DDS administration to male and female rats (30 mg/kg body wt, twice a day, for 4 days) on liver oxidative stress through assessment of biliary output and liver content of reduced (GSH) and oxidized (GSSG) glutathione, lipid peroxidation, and expression/activities of the main antioxidant enzymes glutathione peroxidase, superoxide dismutase, catalase and glutathione S-transferase. The influence of DDS treatment on expression/activity of the main DDS phase-II-metabolizing system, UDP-glucuronosyltransferase (UGT), was additionally evaluated. The involvement of dapsone hydroxylamine (DDS-NHOH) generation in these processes was estimated by comparing the data in male and female rats since N-hydroxylation of DDS mainly occurs in males. Our studies revealed an increase in the GSSG/GSH biliary output ratio, a sensitive indicator of oxidative stress, and in lipid peroxidation, in male but not in female rats treated with DDS. The activity of all antioxidant enzymes was significantly impaired by DDS treatment also in male rats, whereas UGT activity was not affected in any sex. Taken together, the evidence indicates that DDS induces oxidative stress in rat liver and that N-hydroxylation of DDS was the likely mediator. Impairment in the activity of enzymatic antioxidant systems, also associated with DDS-NHOH formation, constituted a key aggravating factor.     

Effects of vanadate on male rat reproductive tract histology, oxidative stress markers and androgenic enzyme activities

Vanadium has been recognized as industrial hazards that adversely affect male reproductive systems of humans and animals. However, less information is available concerning the underlying mechanism in the pathogenesis of male reproductive dysfunction. The present study investigated the possible involvement of oxidative stress to induce oxidative deterioration of testicular functions in adult rats. The results of in vitro and in vivo studies demonstrate that vanadium treatment resulted in a significant dose- and time-dependent increase in the testicular lipid peroxidation, marked inhibition in the level of superoxide dismutase and catalase activities, decreased sperm counts, and substantially inhibited the activities of Delta(5)3beta- and 17beta-hydroxysteroid dehydrogenase as well as serum testosterone level. Histopathological examination revealed inhibition of spermatogenesis and the preferential loss of maturing and elongated spermatids along with increased percent of abnormal sperm. Taken together, the results suggest that an increase in free radical formation relative to loss of antioxidant defense system during vanadium exposure may render testis more susceptible to oxidative damage leading to their functional inactivation. Thus the toxic effects of vanadium are cumulative and that vanadium produced damages in testes are dose- and time-dependent.     

Genotoxicity and oxidative stress in fish after a short-term exposure to silver nanoparticles

This study examined the effects of waterborne silver nanoparticles (AgNPs) on juvenile fish Piaractus mesopotamicus (“pacú”), and analyzed toxicological endpoints such as metal burdens, oxidative stress and genotoxicity in a short-term assay. Fish were individually exposed to 0 (control), 2.5, 10, and 25 μg AgNPs/L. After 24 h, silver accumulation was greater in the brain than the liver and gills at all silver concentrations. Fish exposed to higher AgNPs concentrations showed major alterations in oxidative stress markers. An increase in lipid peroxidation (LPO) levels was observed in the liver of fish exposed to 10 μg AgNPs/L with no changes in the antioxidant enzymes activities. In the case of the 25 μg AgNPs/L treatment, a hepatic activation of the enzymatic antioxidant defense occurred, and LPO levels resulted unaltered. On the other hand, the brain presented the highest LPO levels at both 10 and 25 μg AgNPs/L exposures. The AgNPs toxicity was also evidenced by the DNA damage in fish erythrocytes at higher concentrations. Summarizing, a short exposure to sublethal concentrations of AgNPs is enough to generate deleterious effects on fish, including DNA damage.     

Tryptophan loading induces oxidative stress

In previous studies tryptophan loads have been administered to human subjects in order to raise central levels of 5-hydroxytryptamine (5HT) and assess the effects of 5HT on behaviour and mood. However, tryptophan is metabolised primarily along the oxidative kynurenine pathway. In this study a 6 g oral tryptophan load was administered to 15 healthy volunteers and the levels of kynurenines and lipid peroxidation products (indicative of oxidative stress) were measured. The results demonstrate that tryptophan loading produces a highly significant increase in lipid peroxidation products in parallel with increased kynurenines. The oxidative stress may result from the generation of quinolinic acid, 3-hydroxykynurenine, and 3-hydroxyanthranilic acid, all of which are known to have the ability to generate free radicals. The results may have implications for the use of tryptophan loading in psychiatric practice, and for the chronic use of diets high in tryptophan.     

Ameliorating effects of troxerutin on nickel-induced oxidative stress in rats

Abstract

Objective

This study investigates the effects of troxerutin on nickel (Ni)-induced oxidative stress in rats.

Methods

Nickel as nickel sulfate (20 mg/kg body weight (b.w.)) was administered intraperitoneally for 20 days to induce toxicity in the subject rats. The levels of stress markers AST, ALT, ALP, LDH, and GGT in the hepatic tissue were significantly increased while a decrease in the levels of enzymic and non-enzymic antioxidants was observed in Ni intoxicated rats.

Results

Oral administration of troxerutin along with Ni for 20 days in a dose-dependent manner significantly reverted the stress markers in the liver tissue to near normal level. Troxerutin exhibited significant protection at 100 mg/kg b.w. Histopathological studies also supported the above findings.

Conclusions

Thus, we conclude that troxerutin preserved the histo-architecture and ameliorated stress markers in the liver tissue of Ni-intoxicated rats.     

No evidence for oxidative stress as a mechanism of action of hyperhomocysteinemia in humans

Oxidative stress has been suggested as one of the physiopathologic conditions underlying the association of total plasma homocysteine (p-tHcy) with cardiovascular disease (CVD), but this hypothesis has not been validated in human epidemiological studies. We measured plasma and erythrocyte antioxidant enzymes glutathione peroxidase (GPx) and superoxide dismutase (SOD), along with serum lipid-soluble antioxidants alpha-tocopherol, beta-carotene, lycopene and retinol, in a sample of 123 healthy elderly subjects (54 men, 69 women). Plasma malondialdehyde (p-MDA) was determined as a marker of lipid peroxidation, and p-tHcy was quantified by HPLC. No significant differences were found for p-MDA, GPx or SOD activities or serum antioxidant concentrations, in subjects with elevated p-tHcy (≥15 μmol/l) as compared to those with lower plasma homocysteine. Hyperhomocysteinemia did not lead to increased risk of having the highest p-MDA values, in either sex. We found no evidence that p-tHcy was associated with lipid peroxidation in this elderly human sample. Our results do not support the view that hyperhomocysteinemia would induce an adaptive response of antioxidant systems, either. More epidemiologic and clinical research is needed to clarify whether homocysteine promotes atherosclerosis by means of an oxidative stress mechanism.     

Oxidative stress and antioxidant defense responses by goldfish tissues to acute change of temperature from 3 to 23 °C

The effects of a rapid transfer from a low (3 °C) to a warm (23 °C) temperature on oxidative stress markers and antioxidant defenses were studied in the brain, liver and kidney of the goldfish, Carassius auratus. Cold-acclimated fish were acutely moved to 23 °C and sampled after 1, 6, 12, 24, 48 or 120 h of warm temperature exposure. Lipid peroxide levels increased quickly during the first few hours at 23 °C, but thiobarbituric acid-reactive substances changed little. Protein carbonyl content was reduced by 20–40% in the liver over the entire experimental course, but increased transiently in the kidney. The content of high-molecular mass thiols decreased by two-thirds in the brain and was affected slightly in other organs. By contrast, total low-molecular mass thiols (e.g. glutathione and others) increased transiently. Activities of the primary antioxidant enzymes—superoxide dismutase and catalase—were generally unaffected in goldfish organs, whereas glutathione-dependent enzymes were elevated in the brain and kidney after 24–48 h at 23 °C. Glutathione peroxidase increased by 1.5–2.3-fold and glutathione-S-transferase by 1.7-fold. Hence, a short-term exposure to warm temperature disturbed several oxidative stress markers, but only slightly affected the activities of antioxidant enzymes. However, comparison of the current data for cold-acclimated winter fish with the same parameters in summer fish suggests that longer exposure to high ambient temperature requires the enhancement of activities of glutathione-dependent enzymes for maintaining the steady-state levels lipid peroxidation and protein oxidation in goldfish tissues.     

Heat shock induces oxidative stress in rotan Perccottus glenii tissues

The effects of temperature transition from 19 to 32 °C on oxidative stress indices and activities of the main antioxidant enzymes were investigated in the rotan, Perccottus glenii. Levels of lipid peroxides (LOOH), thiobarbituric acid-reactive substances (TBARS), low- (L-SH) and high-molecular mass (H-SH) thiols and activities of superoxide dismutase (SOD) and catalase were measured in rotan brain, liver and muscle over 1–12 h of high-temperature exposure followed by 3 or 24 h lower (19 °C) temperature recovery. Heat shock exposure during 1 h transiently increased 1.5–3.2-fold LOOH levels in rotan tissues with subsequent suppression of their content; however, 12 h exposure again increased LOOH levels in the brain. TBARS content were elevated by 2–3-fold during the entire heat shock exposure in the brain and liver. Levels of both products of lipid peroxidation were generally near control values during return to 19 °C. L-SH content was lowered during heat shock exposure in the brain, transiently increased after 6 h in the liver and almost disappeared after longer treatment in the muscle. Liver H-SH content slightly decreased under heat shock exposure, but was elevated after 6 h in the brain and muscle. In the latter case, L-SH level was below control values during recovery. SOD activities increased 2-fold in the liver after 6–12 h heat shock. Liver catalase activities decreased at the same conditions. Generally, a quick response to suppression of lipid peroxidation and possible involvement of its products in the up-regulation of antioxidant enzymes seem to be key adaptations to high temperature.     

Hypobaric hypoxia induces oxidative stress in rat brain

High altitude exposure results in decreased partial pressure of oxygen and an increased formation of reactive oxygen and nitrogen species (RONS), which causes oxidative damage to lipids, proteins and DNA. Exposure to high altitude appears to decrease the activity and effectiveness of antioxidant enzyme system. The antioxidant system is very less in brain tissue and is very much susceptible to hypoxic stress. The aim of the present study was to investigate the time dependent and region specific changes in cortex, hippocampus and striatum on oxidative stress markers on chronic exposure to hypobaric hypoxia. The rats were exposed to simulated high altitude equivalent to 6100 m in animal decompression chamber for 3 and 7 days. Results indicate an increase in oxidative stress as seen by increase in free radical production, nitric oxide level, lipid peroxidation and lactate dehydrogenase levels. The magnitude of increase in oxidative stress was more in 7 days exposure group as compared to 3 days exposure group. The antioxidant defence system such as reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and reduced/oxidized glutathione (GSH/GSSG) levels were significantly decreased in all the three regions. The observation suggests that the hippocampus is more susceptible to hypoxia than the cortex and striatum. It may be concluded that hypoxia differentially affects the antioxidant status in the cortex, hippocampus and striatum.     

Carboxyfullerene prevents iron-induced oxidative stress in rat brain

Carboxyfullerene, a water-soluble carboxylic acid derivative of a fullerene, was investigated as a protective agent against iron-induced oxidative stress in the nigrostriatal dopaminergic system of anesthetized rats. Intranigral infusion of exclusive carboxyfullerene did not increase lipid peroxidation in substantia nigra or deplete dopamine content in striatum. Infusion of ferrous citrate (iron II) induced degeneration of the nigrostriatal dopaminergic system. An increase in lipid peroxidation in substantia nigra as well as decreases in K+-evoked dopamine overflow and dopamine content in striatum were observed 7 days after the infusion. Co-infusion of carboxyfullerene prevented iron-induced oxidative injury. Furthermore, tyrosine hydroxylase-immunoreactive staining showed that carboxyfullerene inhibited the iron-induced loss of the dopaminergic nerve terminals in striatum. The antioxidative action of carboxyfullerene was verified by in vitro studies. Incubation of brain homogenates increased the formation of the Schiff base fluorescent products of malonaldehyde, an indicator of lipid peroxidation. Both autooxidation (without exogenous iron) and iron-induced elevation of lipid peroxidation of brain homogenates were suppressed by carboxyfullerene in a dose-dependent manner. Our results suggest that intranigral infusion of carboxyfullerene appears to be nontoxic to the nigrostriatal dopaminergic system. Furthermore, the potent antioxidative action of carboxyfullerene protects the nigrostriatal dopaminergic system from iron-induced oxidative injury.     

Hypoxia induces oxidative stress in tissues of a goby, the rotan Perccottus glenii

The effects of hypoxia (0.4 mg O₂/L) for 2, 6 or 10 h and subsequent normoxic recovery on the levels of lipid peroxides, thiobarbituric acid reactive substances, protein carbonyls (CP), free thiols, and the activities of six antioxidant and associated enzymes were measured in the brain, liver, and skeletal muscle of the rotan Perccottus glenii. Hypoxia increased CP content in the brain (5.0–7.4-fold), liver (2.2–3.3-fold) and muscle (3.2–61-fold) relative to controls and the levels remained elevated during recovery. Lipid peroxide content rose within 2 h of hypoxia in all tissues examined with the most marked increase (8.7-fold) in the liver, but decreased again during longer hypoxic exposure except in the muscle. Levels of low-molecular mass thiols were transiently lowered after 2 h hypoxia in all tissues, but were higher compared with controls after longer hypoxic exposure and recovery. Hypoxia decreased protein thiol content in the liver and muscle that return to control levels during recovery. Experimental conditions affected enzyme activities in a different manner. Superoxide dismutase activity rose two-fold in the liver of hypoxic fish, and a similar tendency was seen in muscle glutathione-S-transferase. Activities of other enzymes were decreased or unchanged during hypoxia and elevated in some cases during normoxic recovery. Taken together, these data show that hypoxia resulted in the development of oxidative stress and a compensatory changes of antioxidant enzymes in the tissues.     

微囊藻细胞抽提物亚慢性暴露导致小鼠肝脏氧化应激

研究了微囊藻细胞抽提物亚慢性暴露对小鼠肝脏抗氧化系统的影响.采用腹腔注射进行连续染毒28d,染毒组剂量为3.3μg micmcystins/kg体重.结果显示,超氧化物歧化酶、过氧化氧酶、谷胱甘肽过氧化物酶在第4周时发生显著性升高,提示微囊藻细胞抽提物激活了小鼠肝脏抗氧化系统.谷胱甘肽-S-转移酶和对照组相比也显著提高,表明谷胱甘肽-S-转移酶作为解毒Ⅰ相酶加快了对肝脏微囊藻毒素的清除.脂质过氧化产物丙二醛也显著升高,说明抗氧化系统未能清除微囊藻细胞抽提物对小鼠肝脏的氧化损伤,导致了氧化应激的产生.结果表明低剂量微囊藻细胞抽提物长时间暴露能够导致小鼠肝脏氧化损伤.     

Drought induces oxidative stress in pea plants

Pea (Pisum sativum L. cv. Frilene) plants subjected to drought (leaf water potential of -1.3 MPa) showed major reductions in photosynthesis (78), transpiration (83), and glycolate oxidase (EC 1.1.3.1) activity (44), and minor reductions (18) in the contents of chlorophyll a, carotenoids, and soluble protein. Water stress also led to pronounced decreases (72–85) in the activities of catalase (EC 1.11.1.6), dehydroascorbate reductase (EC 1.8.5.1), and glutathione reductase (EC 1.6.4.2), but resulted in the increase (32–42) of non-specific peroxidase (EC 1.11.1.7) and superoxide dismutase (EC 1.15.1.1). Ascorbate peroxidase (EC 1.11.1.11) and monodehydroascorbate reductase (EC 1.6.5.4) activities decreased only by 15 and the two enzymes acted in a cyclic manner to remove H₂O₂, which did not accumulate in stressed leaves. Drought had no effect on the levels of ascorbate and oxidized glutathione in leaves, but caused a 25 decrease in the content of reduced glutathione and a 67 increase in that of vitamin E. In leaves, average concentrations of catalytic Fe, i.e. Fe capable of catalyzing free-radical generation by redox cycling, were estimated as 0.7 to 7 M (well-watered plants, depending on age) and 16 M (water-stressed plants); those of catalytic Cu were 4.5 M and 18 M, respectively. Oxidation of lipids and proteins from leaves was enhanced two- to threefold under stress conditions and both processes were highly correlated. Fenton systems composed of the purported concentrations of ascorbate, H₂O₂, and catalytic metal ions in leaves produced hydroxyl radicals, peroxidized membrane lipids, and oxidized leaf proteins. It is proposed that augmented levels and decompartmentation of catalytic metals occurring during water stress are responsible for the oxidative damage observed in vivo.Abbreviations and Symbol ASC ascorbate - DW dry weight - DHA dehydroascorbate - GSH reduced glutathione - GSSG oxidized glutathione - MDHA monodehydroascorbate (ascorbate free radical) - SOD Superoxide dismutase - _wa water potential We thank Dr. R. Picorel (E.E. de Aula Dei, CSIC) for allowing us access to HPLC equipment. J.F.M., 1.1., and S.F. were the recipients of predoctoral fellowships from the Comunidades Autónomas de Aragon, Pais Vasco, and Navarra, respectively. R.V.K. thanks the U.S. Department of Agriculture (grant 91-37305-6705) for travel support. This work was financed by grants from the Comisión Interministerial de Ciencia y Tecnología (AGR-91-0857-C02 to P.A. and M.B.) and the Dirección General de Investigación Científica y Técnica (PB92-0058 to M.B) of Spain.     

The effects of dietary restriction on oxidative stress in rodents

Oxidative stress is observed during aging and in numerous age-related diseases. Dietary restriction (DR) is a regimen that protects against disease and extends life span in multiple species. However, it is unknown how DR mediates its protective effects. One prominent and consistent effect of DR in a number of systems is the ability to reduce oxidative stress and damage. The purpose of this review is to comprehensively examine the hypothesis that dietary restriction reduces oxidative stress in rodents by decreasing reactive oxygen species (ROS) production and increasing antioxidant enzyme activity, leading to an overall reduction of oxidative damage to macromolecules. The literature reveals that the effects of DR on oxidative stress are complex and likely influenced by a variety of factors, including sex, species, tissue examined, types of ROS and antioxidant enzymes examined, and duration of DR. Here we present a comprehensive review of the existing literature on the effect of DR on mitochondrial ROS generation, antioxidant enzymes, and oxidative damage. In a majority of studies, dietary restriction had little effect on mitochondrial ROS production or antioxidant activity. On the other hand, DR decreased oxidative damage in the majority of cases. Although the effects of DR on endogenous antioxidants are mixed, we find that glutathione levels are the most likely antioxidant to be increased by dietary restriction, which supports the emerging redox-stress hypothesis of aging.     

4-Hydroxynonenal induces oxidative stress and death of cultured spinal cord neurons

Primary spinal cord trauma can trigger a cascade of secondary processes leading to delayed and amplified injury to spinal cord neurons. Release of fatty acids, in particular arachidonic acid, from cell membranes is believed to contribute significantly to these events. Mechanisms of fatty acid-induced injury to spinal cord neurons may include lipid peroxidation. One of the major biologically active products of arachidonic acid peroxidation is 4-hydroxynonenal (HNE). The levels of HNE-protein conjugates in cultured spinal cord neurons increased in a dose-dependent manner after a 24-h exposure to arachidonic acid. To study cellular effects of HNE, spinal cord neurons were treated with different doses of HNE, and cellular oxidative stress, intracellular calcium, and cell viability were determined. A 3-h exposure to 10 microM HNE caused approximately 80% increase in oxidative stress and 30% elevation of intracellular calcium. Exposure of spinal cord neurons to HNE caused a dramatic loss of cellular viability, indicated by a dose-dependent decrease in MTS [3-(4, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-s ulfophenyl)- 2H-tetrazolium, inner salt] conversion. The cytotoxic effect of HNE was diminished by pretreating neurons with ebselen or N-acetylcysteine. These data support the hypothesis that formation of HNE may be responsible, at least in part, for the cytotoxic effects of membrane-released arachidonic acid to spinal cord neurons.     

Therapy refractory hypertension in adults: aortic coarctation has to be ruled out

In patients with unexplained hypertension, especially in combination with a cardiac murmur, the presence of an aortic coarctation should always be ruled out given the high morbidity and mortality. However, particularly patients with an isolated coarctation often remain asymptomatic for years and the defect may be unnoticed even until the fifth or sixth decade of life. In the present article, we describe two patients with late detected coarctation to illustrate the clinical consequences, diagnostic clues for earlier detection and current therapeutic options to achieve optimal treatment. The key sign of an aortic coarctation, a difference in arterial blood pressure measured between the upper and lower extremities, should always be examined, followed by echocardiography. We conclude that even in case of a late detected severe coarctation, surgical or percutaneous repair has proven to be feasible and substantially effective, improving quality of life and lowering the risk of further hypertension-associated problems.     

Beneficial effects of DL-alpha-lipoic acid on cyclophosphamide-induced oxidative stress in mitochondrial fractions of rat testis

The present study investigated the protective efficacy of dl-alpha-lipoic acid on the peroxidative damage and abnormal antioxidant levels in the mitochondrial fraction of testis in cyclophosphamide (CP) administered rats. Male Wistar rats of 140+/-20 g were categorized into four groups. Two groups were administered CP (15 mg/kg body weight once a week for 10 weeks by oral gavage) to induce testicular toxicity; one of these groups received lipoic acid treatment (35 mg/kg body weight intraperitoneally once a week for 10 weeks, 24 h prior to CP administration). A vehicle-treated control group and a lipoic acid drug control group were also included. The mitochondrial fraction of untreated CP-exposed testis showed 1.84-fold increase in lipid peroxidation, along with a significant (P<0.001) increase in hydrogen peroxide levels. In CP-exposed rats, we observed abnormal changes in the activities/levels of mitochondrial enzymic (superoxide dismutase, glutathione peroxidase and glutathione reductase) and non-enzymic (reduced glutathione, ascorbate and alpha-tocopherol) antioxidants. CP-treated rats also showed decline in the activities of mitochondrial enzymes such as succinate dehydrogenase, malate dehydrogenase and isocitrate dehydrogenase. In contrast, rats pretreated with lipoic acid showed normal lipid peroxidation and antioxidant defenses, thereby showing the protection rendered by lipoic acid.     

Arbuscular mycorrhizal fungi regulate the oxidative system,hormones and ionic equilibrium to trigger salt stress tolerance in Cucumis sativus L.

Arbuscular mycorrhizal fungi (AMF) association increases plant stress tolerance. This study aimed to determine the mitigation effect of AMF on the growth and metabolic changes of cucumbers under adverse impact of salt stress. Salinity reduced the water content and synthesis of pigments. However, AMF inoculation ameliorated negative effects by enhancing the biomass, synthesis of pigments, activity of antioxidant enzymes, including superoxide dismutase, catalase, ascorbate peroxidase and glutathione reductase, and the content of ascorbic acid, which might be the result of lower level lipid peroxidation and electrolyte leakage. An accumulation of phenols and proline in AMF-inoculated plants also mediated the elimination of superoxide radicals. In addition, jasmonic acid, salicylic acid and several important mineral elements (K, Ca, Mg, Zn, Fe, Mn and Cu) were enhanced with significant reductions in the uptake of deleterious ions like Na+. These results suggested that AMF can protect cucumber growth from salt stress.     

Markers for oxidative stress associated with soft rots in French beans (Phaseolus vulgaris) infected by Botrytis cinerea

The role of active oxygen species has been studied in spreading soft-rot lesions caused by the necrotrophic fungal pathogen Botrytis cinerea Pers.:Fr. in leaves of four genotypes of French bean (Phaseolus vulgaris L.). Large increases were observed for the aldehydic end-products of oxidative damage, malondialdehyde and 4-hydroxy-2-nonenal, as a result of infection in each of the genotypes studied. Similar increases were found in a stable free radical and g=4.27 Fe(III) signals, but not Mn(II) signals, in electron paramagnetic resonance spectra. These changes were accompanied by large decreases in ascorbic acid levels, with changes in the antioxidant glutathione being genotype dependent. Received: 3 May 2000 / Accepted: 13 July 2000     

Tissue-specific oxidative stress responses in fish exposed to 2,4-D and azinphosmethyl

Species- and tissue-specific defenses against the possibility of oxidative stress and lipid peroxidation were compared in adult fish, Oreochromis niloticus and Cyprinus carpio, exposed to 2,4-dichlorophenoxyacetic acid (2,4-D), azinphosmethyl and their combination for 96 h. Superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase activities were monitored in kidney, brain and gill. In all exposure groups there was a marked increase in SOD activity in gill tissues in both fish species, while it was at the control level in other tissues. The highest elevation of SOD activity by combined treatment was observed in C. carpio. Individual and combined treatments caused an elevation in catalase and GPx activities in kidney of C. carpio. Catalase activity was unaffected in brain of O. niloticus, while GPx activity was decreased after all treatments. Glutathione S-transferase (GST) activity was higher than the control levels in kidney of both fish exposed to pesticides. No significant changes were observed in malondialdehyde level in kidney and brain of C. carpio. Our results indicate that the toxicities of azinphosmethyl and 2,4-D may be related to oxidative stress. Also, the results show that SOD activity in gill and GST activity in kidney may be used as biomarkers for pollution monitoring and indicate that the activities of certain biomarkers in C. carpio are more sensitive to pesticides than those in O. niloticus.