The effects of fucoidan extracts on CCl<Subscript>4</Subscript>-induced liver injury

The aim of this study was to elucidate the antioxidant properties of fucoidan extracts (FE) against CCl(4)-induced oxidative stress by monitoring the levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Female, Sparague-Dowley rats were administered with FE (100 mg/kg daily) for 14 days and CCl(4) on the 15'th day, 12 h before they were sacrificed. The levels of GOT, GPT, ALP and LDH in serum of rats, as well as the levels of MDA, SOD, CAT and GPx in total liver homogenate were analyzed. CCl(4)-treatment was found to increase the levels of GOT, GPT, ALP, LDH and MDA, as well as decrease levels of SOD, CAT and GPx significantly. The pre-treatment of rats with FE, however, suppressed the increment of levels of GOT, GPT, ALP, LDH and MDA, as well as recovered the levels of SOD, CAT and GPx in CCl(4)-treated rats. Moreover there was a significant decrease in incidences of necrosis and cirrhosis in the liver tissue of FE-treated rats. These results implied that FE possessed antioxidant properties against CCl(4)-induced oxidative stress.     

Oxidative stress in ovariectomy menopause and role of chondroitin sulfate

Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. Mitochondria are especially important in the oxidative stress as ROS have been found to be constantly generated as an endogen threat. Mitochondrial defense depends mainly on superoxide dismutase (SOD) and glutathione peroxidase (GPx), whereas microsomal defense depends on catalase (CAT), which is an enzyme abundant in microsomes. SOD removes superoxide anions by converting them to H2O2, which can be rapidly converted to water by CAT and GPx. Also, GPx converts hydroperoxide (ROOH) into oxidized-glutathione (GSSG). Ovariectomized (OVX) rats are used as an oxidative stress model. An ovariectomy increased the levels of MDA, one of the end-products in the lipid peroxidative process, and decreased levels of the antioxidative enzymes; SOD, CAT and GPx. However, Chondroitin sulfate (CS) decreased the levels of MDA, but increased the levels of SOD, CAT and GPx in a dose-dependent manner. Moreover, inflammation and cirrhosis of liver tissue in CS- treated rats were significantly decreased. These results suggest that CS might be a potential candidate as an antioxidative reagent.     

Influence of dietary ginger (Zingiber officinales Rosc) on oxidative stress induced by malathion in rats.

Pesticide chemicals may induce oxidative stress leading to generation of free radicals and alterations in antioxidants or oxygen free radical (OFR) scavenging enzymes. Hence, the effect of subchronic malathion (O,O-dimethyl-S-1,2, bis ethoxy carbonyl ethyl phosphorodithioate) exposure was evaluated on lipid peroxidation, glutathione and related enzymes and OFR scavenging enzymes in albino rats. Administration of malathion (20 ppm) for 4 weeks increased the malondialdehyde (MDA) levels in serum, activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in erythrocytes and glutathione reductase (GR) and glutathione S-transferase (GST) in serum. However, it decreased the glutathione (GSH) level in whole blood. Concomitant dietary feeding of Zingiber officinales Rosc (ginger 1%, w/w) significantly attenuated malathion induced lipid peroxidation and oxidative stress in these rats. These results indicate the possible involvement of free radicals in organophosphate-induced toxicity and highlight the protective action of ginger, an indigenous medicinal plant product.     

Malathion-induced oxidative stress in human erythrocytes and the protective effect of vitamins C and E in vitro

Malathion is an organophosphate (OP) pesticide that has been shown to induce oxidative stress in erythrocytes through the generation of free radicals and alteration of the cellular antioxidant defense system. We examined the effect of several different doses of malathion (25, 75, 200 microM), or malathion in combination with vitamin C (VC; 10 microM) or vitamin E (VE; 30 microM), on the levels of malondialdehyde (MDA), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in human erythrocytes in vitro. Erythrocytes were incubated under various treatment conditions (malathion alone, vitamins alone, or malathion plus vitamin) at 37 degrees C for 60 min, and the levels of MDA, and SOD, CAT and GPx activities, were determined. Treatment with malathion alone increased the levels of MDA and decreased SOD, CAT, and GPx activities in erythrocytes (P < 0.05). There were no statistical differences among VC-treated, VE-treated, or VC + VE-treated erythrocyes, as compared with nontreated control cells. Treatment of cells with malathion + VC, malathion + VE, or a combination of all three agents prevented malathion-induced changes in antioxidant enzyme activity and lipid peroxidation. However, this effect was seen only at low concentrations of malathion (25 and 75 microM), and the combination of VC + VE had a more protective effect than VC or VE alone. These results indicated that the presence of vitamins at concentrations that are similar to the levels found in plasma have no effect on malathion-induced toxicity in erythrocytes at a concentration of malathion (200 microM) that is typically used in pesticides.     

The effect of chondroitin sulfate against CCl4-induced hepatotoxicity

This study was conducted to develop a new biomaterial to be used for an antioxidative drug. In this study, the hepatoprotective effect of chondroitin sulfate (CS) (100 mg/kg and 200 mg/kg body weight) was investigated at the antioxidative enzyme levels of liver total homogenate and mitochondria fraction. And the carbone tetrachloride (CCl(4))-induced rats were used as hepatotoxic models. The CCl(4) induced rat has been widely used as a hepatotoxic model due to its practicality, convenience and cost effectiveness since the generation of free oxygen radicals by CCl(4) injection was proposed as an important causative agent of hepatotoxicity. Malondialdehyde (MDA) levels were determined as well as the activities of superoxide dismutase (SOD), catalase (CAT), reduced-glutathione (GSH), oxidized-glutathione (GSSG) and glutathione peroxidase (GPx) in the liver. In addition, histopathology of liver tissue was investigated. Liver antioxidative enzyme activity was elevated while MDA concentration was decreased in all CS treated animals. The results demonstrated that CS protected oxidative stress in a dose dependent manner. Moreover, inflammation and cirrhosis in liver tissue of CS treated group were significantly decreased. It gave us an impression that CS might be a radical scavenger.     

Biochemical evidence for free radical-induced lipid peroxidation as a mechanism for subchronic toxicity of malathion in blood and liver of rats

Organophosphorus compounds may induce oxidative stress leading to generation of free radicals and alterations in antioxidant and scavengers of oxygen free radicals (OFRs). The effect of subchronic exposure to malathion in the production of oxidative stress was evaluated in male Wistar rats. Administration of malathion (100, 316, 1000, 1500 ppm) for 4 weeks increased catalase (CAT), superoxide dismutase (SOD) activities as well as malondialdehyde (MDA) concentration in red blood cells (RBC) and liver. However, acetylcholinesterase (AChE) and cholinesterase (ChE) activities were decreased in these samples. The increase in RBC and liver lipid peroxidation correlated well with the inhibition in RBC AChE and liver ChE activities. Elevation of MDA concentrations and increased activities of CAT and SOD showed significant correlations in both RBC and liver samples when different doses of malathion were used. The results of the present study suggest the usefulness of RBC AChE measurement as a good biomarker in the estimation of malathion-induced oxidative stress affecting blood and liver.     

The role of vitamin C as antioxidant in protection of oxidative stress induced by imidacloprid

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 imidacloprid toward male mice and the oxidative stress of the sublethal dose (1/10 LD₅₀) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and activities of the antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-s-transferase (GST). Also, the protective effect of vitamin C (200 mg/kg bw) 30 min before or after administration of imidacloprid were investigated. The results demonstrated that the median lethal dose (LD₅₀) of imidacloprid after 24 h was 149.76 mg/kg bw. The oral administration of 14.976 mg/kg imidacloprid significantly caused elevation in LPO level and the activities of antioxidant enzymes including CAT, SOD, GPx and GST. However, G6PD activity remained unchanged, while the level of GSH content was decreased. In addition, the results showed that vitamin C might ameliorate imidacloprid-induced oxidative damage by decreasing LPO and altering antioxidant defense system in liver. The protective effect of the pre-treatment with vitamin C against imidacloprid-induced oxidative stress in liver mice is better than the post-treatment.     

Effects of trichlorfon on malondialdehyde and antioxidant system in human erythrocytes

Organophosphorus insecticides may induce oxidative stress leading to generation of free radicals and alteration in antioxidant system. The aim of this study was to examine the potency of trichlorfon, an organophosphate insecticide, to induce oxidative stress response in human erythrocytes in vitro. For this purpose trichlorfon solutions in different concentrations and erythrocyte solutions were incubated at 37 °C for 60 min. At the end of the incubation time, malondialdehyde (MDA), an end product of lipid peroxidation, total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes were determined by spectrophotometric methods. Trichlorfon increased MDA formation depended on the concentration. On the other hand, decreases in the GSH-Px activity, GSH levels and increases in the total glutathione levels, SOD and CAT activities were seen in the studied concentrations. The present findings indicate that the in vitro toxicity of trichlorfon may be associated with oxidative stress.     

Protective effect of salvianic acid a on acute liver injury induced by carbon tetrachloride in rats

Previous research has shown that salvianic acid A [2-(3,4-dihydroxyphenyl)-2-hydroxy-propanoic acid, SA] extracted from Salvia miltiorrhiza BGE (Danshen) markedly inhibits lipid peroxidation of mitochondrial membrane of hepatic cells in vitro. The present study was conducted to examine protective effect of SA on liver injury induced by carbon tetrachloride (CCl4) and its possible mechanism in vivo. Male Sprague-Dawley rats weighing 180-200 g were used in the experiments. Five mmol/kg CCl4 in olive oil was given to rats i.p. Spectrophotometrical method was used to measure activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum, activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) as well as malondialdehyde (MDA) level in hepatic tissue and the rate of superoxide anion (O2*-) generation in hepatic submitochondrial particles. Hepatic histological structure was observed under light microscopy. CCl4 caused significant changes of activities of the enzymes, MDA level, and the rate of O2*- generation and histopathological changes of acute hepatic injury were noted. SA reversed the significant changes induced by CCl4. These results demonstrate that SA produces protective action on acute hepatic injury induced by CCl4 via an antioxidative mechanism.     

Evaluation of softwood and hardwood sawmill wastes impact on the common carp "Cyprinus carpio" and its aquatic environment: An oxidative stress study

The aquatic pollution due to sawmill wood wastes constitutes a major threat to hydro-chemical and fauna characteristics of the aquatic ecosystems. When this kind of organics wastes enter aquatic environment it can be taken up by aquatic organisms through respiration and/or through their diet. This could concurrently result in oxidative stress and later having adverse effect on physiological and biochemical function. The importance of fish in the society cannot be over emphasized, hence there is the need to know the influence of sawmill wood wastes on the water quality and fish.Therefore, this work aims to study the impact of five species of wood wastes on a type of fish named common carp (Cyprinus carpio) known as the most widely cultured fish species in the world and on its aquatic environment. The monitoring of water parameters showed deterioration in water quality. The activities of superoxide dismutase (SOD), Catalase (CAT), glutathione peroxidase (GPx) and lipid peroxidation (MDA) were investigated to evaluate the degree of oxidative stress. According to t-student, there was a significant difference compared to control (P < 0.05) in the level of SOD, CAT, GPx and MDA activities in fish exposed to 5 g·l⁻¹ of each sawdust except for GPx, a non-significant difference (p > 0.05) was noted in the case of Beech and Dibetou. When the dispersed amount was about 0.375 g·l⁻¹ we noted a significant difference in the level of SOD and GPx, except for GPx a non-significant difference was detected in the case of Cedar. The level of CAT was significantly difference just in the case of Cedar and Dibetou and that of MDA was significantly difference just in the case of Beech and Mahogany.We conclude therefore that sawmill wood waste not only impact the water quality adversely but also alters the levels of different enzymes activities in Cyprinus Carpio fish by the inhibition of SOD, CAT and GPx activities and by the production of MDA, which reflects response to oxidative stress. This study provides a rational use of these enzymes as suitable biomarkers with different degrees of specificity and as important tool for environmental monitoring.     

Protective effect of Acorus calamus LINN on free radical scavengers and lipid peroxidation in discrete regions of brain against noise stress exposed rat

Exposure to continuous loud noise is a serious health problem due to excess production of oxygen free radicals. In medical research, more attention is paid to the antioxidant properties of medicinal plants to minimize the harmful effects of radicals. The aim of this study was to evaluate the protective effect of both ethyl acetate and methanolic extract of Acorus calamus LINN against noise stress (30 d, 100 dBA/4h/d) induced changes in the rat brain. We measured the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and the levels of reduced glutathione (GSH), vitamin C, vitamin E, protein thiols and lipid peroxidation (LPO) for the evaluation of oxidative stress status in discrete regions of the rat brain like cerebral cortex, cerebellum, pons-medulla, midbrain, hippocampus and hypothalamus. The results indicated that during exposure of noisy environment ROS generation led to increase in corticosterone, LPO and SOD, but decrease in CAT, GPx, GSH, protein thiols, vitamins C and E levels. Both the ethyl acetate and methanolic extract of Acorus calamus protected most of the changes in the rat brain induced by noise-stress.     

Heat stress-induced hepatotoxicity and its prevention by resveratrol in rats

The high ambient temperature beyond the range of comfort zone or thermoneutral zone causes environmental heat stress (HST). It causes serious physiological dysfunction that may result in heat-related diseases and even death. The underlying mechanism in the pathogenesis of hepatic dysfunction following hyperthermic challenge and the possible involvement of oxidative stress to induce oxidative deterioration of liver functions in adult rats are investigated in this study. Cellular damage was assessed in terms of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and histology of liver. The effect of hyperthermia in altering the oxidative stress was evaluated on the basis of its influence on hepatic lipid peroxidation and antioxidant status—superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activity. The current study demonstrated that HST is associated with a complex set of integrated alterations in liver, time-dependent rise in oxidative stress followed by distinct pattern of liver injury in animals. Heat-induced hepatotoxicity was assessed by increased lipid peroxidation, depletion of antioxidant enzyme activities such as SOD, CAT, GPx and tissue damages revealed by hepatic vacuolization, and widespread necrosis. The study also revealed that pretreatment with resveratrol resulted in normalizing these parameters appreciably, emphasizing the therapeutic potentials of this polyphenol. Taken together, the results suggest that an increase in free radical formation relative to loss of the antioxidant defense system during heat stress may render liver more susceptible to oxidative damage, leading to their functional inactivation. However, resveratrol supplementation can be an effective antidote in the treatment of HST-induced malfunction.     

Myricetin suppresses oxidative stress-induced cell damage via both direct and indirect antioxidant action

We evaluated the cytoprotective effect of myricetin on oxidative stress damaged cells by assessment of the scavenging effect of reactive oxygen species (ROS) and the activities of antioxidant enzymes. Myricetin showed the scavenging effect of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals on intracellular ROS. In addition, myricetin restored the activity and protein expression of cellular antioxidant defense enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) reduced by hydrogen peroxide (H(2)O(2)) treatment. H(2)O(2)-induced cellular DNA and lipid damages, and myricetin was found to prevent the DNA damage shown by inhibition of DNA tail and it decreased nuclear phospho-histone H2A.X expression, which are both markers for DNA strand breakage. Membrane lipid peroxidation was also attenuated as shown by inhibition of TBARS formation and of fluorescence intensity of diphenyl-1-pyrenylphosphine (DPPP). These results suggest that myricetin protects cells against H(2)O(2)-induced cell damage via inhibition of ROS generation and activation of antioxidant enzymes.     

Status of lipid peroxidation, glutathione, ascorbic acid, vitamin E and antioxidant enzymes in patients with pregnancy--induced hypertension

The exact pro-oxidant and antioxidant status in pregnancy--induced hypertension patients is still not clear. To add a new insight to the question, changes in the erythrocyte lipid peroxidation products (malondialdehyde; MDA), levels of glutathione (GSH), ascorbic acid and plasma vitamin E (non enzymatic antioxidant parameters) and activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase in erythrocytes were studied in thirty five patients with pregnancy--induced hypertension and thirty five healthy pregnant normotensive cases. It was observed that there was a significant increase in erythrocyte MDA levels, activities of SOD, GPx and a significant decrease in erythrocyte GSH, ascorbic acid, plasma vitamin E levels and catalase activity in patients with pregnancy--induced hypertension when compared to controls. The results of our study have shown higher oxygen free radical production, evidenced by increased levels of MDA and decreased levels of GSH, ascorbic acid, vitamin E and Catalase activity supports the oxidative stress in pregnancy--induced hypertension. The increased activities of antioxidant enzymes may be a compensatory regulation in response to increased oxidative stress. The decreased concentrations of glutathione and antioxidant vitamin status supports the hypothesis that lipid peroxidation is an important causative factor in the pathogenesis of preeclampsia.     

Effects of acute exposure to the radiofrequency fields of cellular phones on plasma lipid peroxide and antioxidase activities in human erythrocytes

Radiofrequency fields of cellular phones may affect biological systems by increasing free radicals, which appear mainly to enhance lipid peroxidation, and by changing the antioxidase activities of human blood thus leading to oxidative stress. To test this, we have investigated the effect of acute exposure to radiofrequency fields of commercially available cellular phones on some parameters indicative of oxidative stress in 12 healthy adult male volunteers. Each volunteer put the phone in his pocket in standby position with the keypad facing the body. The parameters measured were lipid peroxide and the activities of superoxide dismutase (SOD), total glutathione peroxidase (GSH-Px) and catalase. The results obtained showed that the plasma level of lipid peroxide was significantly increased after 1, 2 and 4 h of exposure to radiofrequency fields of the cellular phone in standby position. Moreover, the activities of SOD and GSH-Px in human erythrocytes showed significant reduction while the activity of catalase in human erythrocytes did not decrease significantly. These results indicate that acute exposure to radiofrequency fields of commercially available cellular phones may modulate the oxidative stress of free radicals by enhancing lipid peroxidation and reducing the activation of SOD and GSH-Px, which are free radical scavengers. Therefore, these results support the interaction of radiofrequency fields of cellular phones with biological systems.     

Oxidative stress and genetic damage among workers exposed primarily to organophosphate and pyrethroid pesticides

The indiscriminate use of pesticides in agriculture and public health campaigns has been associated with an increase of oxidative stress and DNA damage, resulting in health outcomes. Some defense mechanisms against free radical‐induced oxidative damage include the antioxidant enzyme systems. The aim of this study was to determine the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and the relationship of antioxidant enzyme levels with DNA damage among sprayers (workers) occupationally exposed to pesticides. The determinations of MDA and antioxidant enzymes were performed spectrophotometrically. The genotoxic effects were evaluated using the comet assay. The results showed a marginally significant decrease in SOD and CAT activities in the high exposure group compared to the control group. For MDA, statistically significant differences were found among people working long term vs. those working temporarily (P = 0.02) as sprayers. In the moderate exposure group, a positive correlation was observed between MDA levels and GPx activity. In the high exposure group, a negative correlation was observed between GR and CAT activities, and between MDA levels and GPx activities. Furthermore, in the high exposure group, a positive correlation between DNA damage parameters and MDA levels was observed. The results suggest an important role of antioxidant enzymes for the protection of DNA damage caused by occupational exposure to pesticides.     

Anti-oxidative and anti-genotoxic effects of carnosine on human lymphocyte culture

The aim of this study was to investigate the effects of carnosine, a biological antioxidant, on the oxidative stress and genotoxicity by a single dose of carbon tetrachloride (CCl(4); 5 mM) in the human lymphocyte culture. We studied the anti-genotoxic effects of carnosine by using sister chromatid exchange (SCE) test system. Also, the anti-oxidative effects of carnosine were evaluated by using superoxide dismutase (SOD), glutathione peroxidase (GPx), total glutathione (GSH) and malondialdehyde (MDA) assay. The SCE frequency was increased when treated with CCl(4). Carnosine at 10 and 20 mM reduced SCE frequency in the human lymphocyte (p < 0.001). In addition, CCl(4) treatment significantly depleted the level of GSH, reduced the activity of SOD and GPx and elevated the level of MDA (p < 0.001). Carnosine treatment led to significant attenuation of CCl(4)-induced oxidative stress by normalization of the activities of SOD and GPx and the level of GSH and MDA (p < 0.05 or 0.001). These results suggest that carnosine could provide anti-oxidative and anti-genotoxic protection for the oxidative and genotoxic agents that cause many diseases including cancer and neurodegenerative disease.     

Adaptive biochemical and physiological responses of <Emphasis Type="Italic">Eriobotrya japonica</Emphasis> to fluoride air pollution

The biochemical and physiological effects of fluoride were investigated in loquat trees (Eriobotrya japonica) grown in the vicinity of a phosphate fertilizer plant in Tunisia. Photosynthetic rate (Pn), stomatal conductance (Gs), transpiration rate (E), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities were assessed; along with photosynthetic pigments, lipid peroxidation, electrolytic leakage (EL) and total phenolic contents in foliage and roots of trees at different distances from the phosphate fertilizer plant. All assessed parameters showed significant discrepancies in comparison with unpolluted sites. Obtained results showed high oxidative stress indices including H₂O₂, lipid peroxidation, and EL, SOD, CAT and GPx activities and proline contents in leaves and roots at the polluted sites as compared to control. In contrast, leaf Pn, Gs, E and photosynthetic pigment contents were low as compared to the control. These results indicate that even though antioxidant responses increased near the factory, adverse effects on physiology were pronounced.     

Antioxidant property of α-asarone against noise-stress-induced changes in different regions of rat brain

Free radicals and other reactive species are considered to be an important causative factor in the development of neurodegenerative diseases. Recent reports have indicated that exposure to loud noise generates excess oxygen free radicals (OFR) in the brain. Antioxidant properties of medicinal plants are attracting more and more research in medicine, to counteract OFR and to minimize the neurodegenerative processes. The drug alpha-asarone (3, 6 and 9 mg kg(-1) body weight, i.p., for 30 days), one of the active principle components of Acorus calamus Linn., was administered intraperitoneally 1/2 h before the animals were exposed to noise-stress (100 dB for 4 h d(-1), for 30 days). We investigated whether 30 days exposure of noise can produce an oxidative stress. Further, if yes then, could alpha-asarone counteract the stress. This was verified by measuring the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), levels of reduced glutathione (GSH), Vitamin C, Vitamin E, protein thiols and lipid peroxidation (LPO) in different regions of the rat brain. All the three doses of alpha-asarone had an effectively protective role by normalizing the increased SOD and LPO, decreased CAT, GPx, GSH, Vitamins C and E and protein thiols due to noise exposure. Thus, action of alpha-asarone against noise-stress may be due its antioxidant property. Our data proved that antioxidant property of alpha-asarone against noise-stress induced changes in the rat brain. Further, more clinical studies are required to investigate effectiveness of the alpha-asarone in noisy environment in human subjects.     

Pro/antioxidant status in young healthy women using oral contraceptives

The aim of the study was to analyze the effects of oral contraceptives (OCs) on pro/antioxidant status in the blood of healthy women aged 20–25 years.Individuals were divided into OCs users and OCs nonusers. Markers of oxidative stress in the blood such as Cu, Cu/Zn ratio, malondialdehyde (MDA), glutathione oxidized (GSSG), and gamma-glutamyl transpeptidase (GGT) were determined. Antioxidants such as glutathione reduced (GSH), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione S-transferase (GST), and superoxide dismutase (SOD) were estimated.Higher Cu concentrations, Cu/Zn ratio and GGT activity in women taking OCs were noted. A significant increase in MDA concentrations in oral OCs users was observed. Heightened activity of CAT in plasma was observed in OCs users, whereas SOD activity remained unchanged in plasma and erythrocyte lysate. A decline of GSH and GSSG in whole blood and glutathiono-dependent enzymes (GPx in plasma, GR in plasma and GST in lysate) was shown.Use of OCs leads to a pro/antioxidant imbalance. The results in the present study confirmed that GGT is an early marker of oxidative stress. Catalase is the main antioxidant, involved in the removal of free radicals in OCs users.