Cytochrome oxidase induction after oxidative stress induced by adriamycin in liver of rats fed with dietary olive oil.

The influence of different kinds of dietary fat (8%) and of endogenous lipid peroxidation with regard to cytochrome c oxidase activity and cytochrome a + a3 concentrations in mitochondria from rat liver has been investigated. It was possible to confirm that the dietary fat induced higher phospholipid degradation in mitochondrial membranes; moreover an endogenous oxidative stress induced by adriamycin was able to increase the peroxidative effects. We have found that the peroxidative effects could sometimes induce an apparent enhancement of cytochrome oxidase activity due to a significant increase of cytochrome a + a3 content. This finding lets us suppose that both changes in the lipid environment and some peroxidation damage could occur in the membrane as a consequence of the fat assumed. Furthermore we should suggest that an induction of the synthesis of cytochrome a + a3 might be related to an enhanced production of peroxides at membrane level.     

Lycopene as a natural protector against gamma-radiation induced DNA damage, lipid peroxidation and antioxidant status in primary culture of isolated rat hepatocytes in vitro

The present study was designed to evaluate the radioprotective effect of lycopene, a naturally occurring dietary carotenoid, on gamma-radiation induced toxicity in cultured rat hepatocytes. The cellular changes were estimated using lipid peroxidative indices like thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), ceruloplasmin, vitamins A, E, C and uric acid. The DNA damage was analysed by single cell gel electrophoresis (comet assay). The increase in the severity of DNA damage was observed with the increase in gamma-radiation dose (1, 2 and 4 Gy) in cultured rat hepatocytes. TBARS were increased significantly whereas the levels of GSH, vitamins C, E and A, ceruloplasmin, uric acid and antioxidant enzymes were significantly decreased in gamma-irradiated groups. The maximum damage to hepatocytes was observed at 4 Gy irradiation. Pretreatment with lycopene (1.86, 9.31 and 18.62 microM) showed a significant decrease in the levels of TBARS and DNA damage. The antioxidant enzymes increased significantly along with the levels of GSH, vitamins A, E, C, uric acid and ceruloplasmin. The maximum protection of hepatocytes was observed at 9.31 muM of lycopene pretreatment. Thus, our results show that pretreatment with lycopene offers protection against gamma-radiation induced cellular damage and can be developed as an effective radioprotector during radiotherapy.     

Antiradical and antioxidant activities of alkaloids isolated from Mahonia aquifolium. Structural aspects

The antioxidant activities of three alkaloids isolated from Mahonia aquifolium--berberine, jatrorrhizine, and magnoflorine--were studied with respect to their structural aspects, particularly the presence and the position of -OH groups, steric conditions of unpaired electron delocalization and parameters of lipophilicity and hydration energy. The antiradical activities of the compounds tested were evaluated as the reactivities toward free stable alpha,alpha'-diphenyl-beta-picrylhydrazyl radical (DPPH). The antioxidant features of the alkaloids tested were investigated in heterogeneous membrane system of DOPC liposomes stressed by peroxidative damage induced by AAPH azoinitiator. Both alkaloids bearing free phenolic groups--jatrorrhizine and magnoflorine--showed better activities in both systems used than berberine not bearing any readily abstractable hydrogen on its skeleton. The former two showed antiperoxidative efficiency in DOPC liposomal membrane comparable to that of an effective scavenger of peroxyl radicals--stobadine-and higher than that of Trolox. We conclude that the favorable antioxidant features of the hydroxylated alkaloids are most probably ensured by the combination of reasonably high antiradical reactivity with high lipophilicity, however, the solvation process was found to markedly interfere with these beneficial effects.     

Lycopene as a natural protector against γ-radiation induced DNA damage,lipid peroxidation and antioxidant status in primary culture of isolated rat hepatocytes in vitro

The present study was designed to evaluate the radioprotective effect of lycopene, a naturally occurring dietary carotenoid, on γ-radiation induced toxicity in cultured rat hepatocytes. The cellular changes were estimated using lipid peroxidative indices like thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), ceruloplasmin, vitamins A, E, C and uric acid. The DNA damage was analysed by single cell gel electrophoresis (comet assay). The increase in the severity of DNA damage was observed with the increase in γ-radiation dose (1, 2 and 4 Gy) in cultured rat hepatocytes. TBARS were increased significantly whereas the levels of GSH, vitamins C, E and A, ceruloplasmin, uric acid and antioxidant enzymes were significantly decreased in γ-irradiated groups. The maximum damage to hepatocytes was observed at 4 Gy irradiation. Pretreatment with lycopene (1.86, 9.31 and 18.62 μM) showed a significant decrease in the levels of TBARS and DNA damage. The antioxidant enzymes increased significantly along with the levels of GSH, vitamins A, E, C, uric acid and ceruloplasmin. The maximum protection of hepatocytes was observed at 9.31 μM of lycopene pretreatment. Thus, our results show that pretreatment with lycopene offers protection against γ-radiation induced cellular damage and can be developed as an effective radioprotector during radiotherapy.     

Protective effect of Piper longum L. on oxidative stress induced injury and cellular abnormality in adriamycin induced cardiotoxicity in rats

Effect of methanolic extract of fruits of P. longum (PLM) on the biochemical changes, tissue peroxidative damage and abnormal antioxidant levels in adriamycin (ADR) induced cardiotoxicity in Wistar rats was investigated. PLM was administered to Wistar albino rats in two different doses, by gastric gavage (250 mg/kg and 500 mg/kg) for 21 days followed by ip ADR (15 mg/kg) on 21st day. ADR administration showed significant decrease in the activities of marker enzymes aspartate transaminase, alanine transaminase, lactate dehydrogenase and creatine kinase in heart with a concomitant increase in their activities in serum. A significant increase in lipid peroxide levels in heart of ADR treated rats was also observed. Pretreatment with PLM ameliorated the effect of ADR on lipid peroxide formation and restored activities of marker enzymes. Activities of myocardial antioxidant enzymes like catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase along with reduced glutathione were significantly lowered due to cardiotoxicity in rats administered with ADR. PLM pretreatment augmented these endogenous antioxidants. Histopathological studies of heart revealed degenerative changes and cellular infiltrations in rats administered with ADR and pretreatment with PLM reduced the intensity of such lesions. The results indicate that PLM administration offers significant protection against ADR induced oxidative stress and reduces the cardiotoxicity by virtue of its antioxidant activity.     

Changes in the function and ultrastructure of vessels in the rat model of multiple low dose streptozotocin-induced diabetes

In this study we investigated functional changes in the femoral artery and ultrastructural alterations in mesenteric vessels and capillaries in the rat model of multiple low dose streptozotocin (STZ)-induced diabetes. Participation of oxidative stress in this model of diabetes was established by studying the effect of the pyridoindole antioxidant stobadine (STB) on diabetes-induced impairment. Experimental diabetes was induced by i.v. bolus of STZ (20 mg/kg) given for three consecutive days to male rats. At the 12(th) week following STZ administration, the animals revealed typical signs of diabetes, such as polyphagia, polydypsia and polyuria. There was no weight gain in the diabetic groups throughout the experiment. No exitus occurred in any group. Diabetes was characterised with high levels of plasma glucose, no significant changes in lipid metabolism, decreased serum levels of glutathione, increased serum levels of the lysosomal enzyme N-acetyl-beta-D-glucosaminidase (NAGA), injured endothelial relaxant capacity of the femoral artery and alterations in ultrastructure of mesenteric arteries and capillaries. Antioxidant STB in the dose of 25 mg/kg body weight i.p. (5 times per week) did not influence glucose levels, however, it mitigated biochemical, functional and ultrastructural changes induced by diabetes, suggesting a role of reactive oxygen species in diabetes-induced tissue damage.     

Response of liver antioxidant system to taurine in rats fed high fructose diet

Fructose-fed rats were more susceptible to peroxidative damage as measured by thiobarbituric acid reactive species. The concentrations of lipid peroxides, diene conjugates, lipofuscin and hydroperoxides were significantly higher. The levels of enzymic antioxidants such as vitamin C, vitamin E and glutathione and activities of antioxidant enzymes were significantly lower in fructose-fed rats. When these rats received taurine in drinking water, peroxidative damage was minimal in both plasma and liver. Taurine was effective in inducing the antioxidant potential in fructose-fed rats. Increased peroxidative damage in liver is likely to be associated with fructose dependent pathology, which could be reduced by taurine by enhancing the antioxidant potential.     

Vitamin E inhibits hepatic oxidative stress, toxicity and hyperproliferation in rats treated with the renal carcinogen ferric nitrilotriacetate

Ferric nitrilotriacetate (Fe-NTA) is a potent renal and hepatic tumor promoter, which acts through a mechanism involving oxidative stress. Fe-NTA when injected intraperitoneally into rats induces hepatic ornithine decarboxylase activity as well as hepatic DNA synthesis. Vitamin E is a well-known, lipid-soluble and chain-breaking antioxidant which protects cell membranes from peroxidative damage. In this study, we investigated the protective effect of vitamin E, a major fat-soluble antioxidant, against Fe-NTA-mediated hepatic oxidative stress, toxicity and hyperproliferation in Wistar rats. Animals were treated with two different doses of vitamin E for 1 week prior to Fe-NTA treatment. Vitamin E at a higher dose of 2.0 mg/animal/day showed significant reduction in Fe-NTA-induced hepatic ornithine decarboxylase activity, DNA synthesis, microsomal lipid peroxidation and hydrogen peroxide generation. Fe-NTA treatment alone caused depletion of glutathione, glutathione metabolizing and antioxidant enzymes in rat liver, whereas pretreatment of animals with vitamin E reversed these changes in a dose-dependent manner. Taken together, our results suggest that vitamin E may afford substantial protection against the damage caused by Fe-NTA exposure and can serve as a potent preventive agent to suppress oxidant-induced tissue injury.     

Interrelation of active oxygen species,membrane damage and altered calcium functions

Incubation of freshly isolated rat liver mitochondria in the presence of oxygen free radical generating hypoxanthine —xanthine oxidase system led to swelling of mitochondria as measured by the change in optical density, which was reversed by the addition of superoxide dismutase. O₂ ^– in the presence of CaCl₂ enhanced the peroxidative decomposition of mitochondrial membrane lipids along with swelling of the organelle. Free radical generation led to enhancement of monoamine oxidase activity while glutathione peroxidase and cytochrome c oxidase were inhibited. Tertbutyl hydroperoxide (t-BHP) caused mitochondrial swelling through oxidative stress. Incorporation of ruthenium red, which is a Ca²⁺ transport blocker, during assay abolished peroxidative membrane damage and swelling. Dithiothreitol (DTT) accorded protection against t-BHP induced mitochondrial swelling. The above in vitro data suggest a possible interrelationship of active oxygen species, membrane damage and calcium dynamics.     

Sodium meta-arsenite induced reactive oxygen species in human red blood cells: impaired antioxidant and membrane redox systems,haemoglobin oxidation,and morphological changes

Arsenic (As) is an air and water toxicant that causes cancer in multiple organs. Humans are exposed to As through contaminated water. We have examined the cytotoxicity of sodium meta-arsenite (SA), an As(III) compound, in human red blood cells (RBC) under in vitro conditions. Haemolysates were prepared from human RBC treated with different concentrations of SA (0.1–5.0?mM) for 5?h at 37?°C. SA treatment of RBC caused significant increase in methaemoglobin formation, protein and lipid oxidation, and nitric oxide levels. It also resulted in decrease in glutathione levels, methaemoglobin reductase activity and plasma membrane redox system. SA exposure also inhibited the pathways of glucose metabolism while increasing AMP deaminase and glyoxalase-I. It impaired the enzymatic and non-enzymatic antioxidant defence systems which resulted in decreased antioxidant power and a compromised ability to quench free radicals. SA exposure also damaged the membrane since it decreased the activity of membrane bound enzymes, increased the osmotic fragility of treated cells and induced gross morphological changes. This cytotoxicity was the result of oxidative damage since the production of reactive oxygen species (ROS) was increased in SA treated erythrocytes. Thus As(III) causes extensive damage to RBC which impairs their antioxidant system and alters the major cellular metabolic pathways. All this has the potential to lower the oxygen carrying capacity of RBC and reduce their lifespan in blood.     

He-Ne激光对增强UV-B辐射下小麦幼苗膜脂过氧化的缓解作用

采用He-Ne激光(5 mW/mm2)辐照增强UV-B辐射(10.08 kJ/m2.d)的晋麦8号小麦幼苗,通过测定小麦幼苗叶片细胞质膜透性、丙二醛(MDA)的含量以及脂氧合酶(LOX)、过氧化氢酶(CAT)、抗坏血酸过氧化物酶(APX)和谷光苷肽过氧化物酶(GPX)的活性变化,研究He-Ne激光对增强UV-B辐射的小麦幼苗膜脂过氧化的影响。结果显示,He-Ne激光辐照可使经UV-B辐射后小麦幼苗叶片质膜相对透性、MDA含量、LOX活性降低,而使CAT、APX和GPX的活性均升高。分析表明UV-B辐射增强可导致膜脂过氧化加剧,而一定剂量的He-Ne激光能够通过促进酶促抗氧化系统酶的活性来缓解紫外线辐射下小麦幼苗的膜脂过氧化作用。     

Vitamin E inhibits hepatic oxidative stress,toxicity and hyperproliferation in rats treated with the renal carcinogen ferric nitrilotriacetate

Abstract

Ferric nitrilotriacetate (Fe-NTA) is a potent renal and hepatic tumor promoter, which acts through a mechanism involving oxidative stress. Fe-NTA when injected intraperitoneally into rats induces hepatic ornithine decarboxylase activity as well as hepatic DNA synthesis. Vitamin E is a well-known, lipid-soluble and chain-breaking antioxidant which protects cell membranes from peroxidative damage. In this study, we investigated the protective effect of vitamin E, a major fat-soluble antioxidant, against Fe-NTA-mediated hepatic oxidative stress, toxicity and hyperproliferation in Wistar rats. Animals were treated with two different doses of vitamin E for 1 week prior to Fe-NTA treatment. Vitamin E at a higher dose of 2.0 mg/animal/day showed significant reduction in Fe-NTA-induced hepatic ornithine decarboxylase activity, DNA synthesis, microsomal lipid peroxidation and hydrogen peroxide generation. Fe-NTA treatment alone caused depletion of glutathione, glutathione metabolizing and antioxidant enzymes in rat liver, whereas pretreatment of animals with vitamin E reversed these changes in a dose-dependent manner. Taken together, our results suggest that vitamin E may afford substantial protection against the damage caused by Fe-NTA exposure and can serve as a potent preventive agent to suppress oxidant-induced tissue injury.     

Radiation induced oxidative stress: I. Studies in Ehrlich solid tumor in mice

Understanding the response of tumors to ionizing radiation might potentially lead to improvement in tumor control and patient morbidity. Since the antioxidant status is likely to be linked to radioresponse, its modulation needs to be examined. Therefore, Swiss albino male mice (7–8 weeks old) with Ehrlich solid tumors were irradiated with different doses of gamma rays (0–9 Gy) at a dose rate of 0.0153 Gy/s; and enzymes involved in antioxidant functions were determined in the tumors. Radiation effects in terms of oxidative damage, LDH, nitric oxide and DNA fragmentation were also examined.In tumors, the specific activity of SOD was increased with dose but declined 6 Gy onwards. GST, DTD and GSH showed an almost progressive increase. These enhanced activities might have resulted from the increased protein expression. This possibility was supported by the Western Blot analysis for GST protein. These changes might be closely linked to the radiation-induced oxidative stress as reflected by the enhanced levels of peroxidative damage, DNA fragmentation, LDH activity and nitric oxide levels. These findings may have relevance to radiation therapy of cancer as the elevated antioxidant status of irradiated tumors is likely to limit the effectiveness of radiation dose and adversely affect the therapeutic gain.     

Effects of combined irradiation and doxorubicin treatment on cardiac function and antioxidant defenses in the rat

Combined radiotherapy and chemotherapy have represented a major advance in the therapeutic management of cancer therapy. However, the combination of doxorubicin (DXR) and cardiac irradiation (IRR) could precipitate the unexpected expression of congestive heart failure. Oxidative lesions induced by IRR and DXR could represent one of the pathogenic factors of myocardial dysfunction. Our investigations were performed to evaluate in the rat: 1) cardiac functional changes, 2) cardiac and plasma peroxidative damage and antioxidant defenses variations, that occur 24 h (acute effects) and 30 d (middle term effects) following DXR treatment 1 mg/kg(-1)/day(-1) IP for 10 d and a 1 x 20 Gy cardiac gamma-irradiation. Our results showed that DXR affected heart reactivity as early as the end of its administration, although irradiation exerted no detectable effect. Antioxidant defenses disturbances in hearts of DXR treated rats were characterized by vitamins C and E decreases, catalase activity induction and an increase in lipid peroxidation. Moreover, plasma vitamin C consumption and the lower level of plasma lipid peroxidation attested to the efficient solicitation of antioxidant defenses that probably contributed to the preservation of cardiac function at 24 h. After 30 d, cardiac dysfunction became symptomatic at rest, resulting from DXR cardiac toxicity. In spite of the persistent activation of cardiac catalase activity, antioxidant deficiency and increased plasma and cardiac lipid peroxidation highlighted defenses overtaken. Thus, different physiopathological mechanisms are involved in heart disturbance at acute and middle terms, IRR and DXR acting on distinct targets without disclosing synergistic effects. After 30 d, cardiac and plasma biochemical abnormalities were emphasized by the combined DXR+IRR therapy, pointing out the severity of the damage. Oxidative damage to the heart induced both by irradiation and DXR, may be one of the pathogenic factors of myocardial dysfunction. There is the possibility that the deleterious effects might be limited by the use of pharmacologic antioxidant agents.     

Lipid peroxidation associated cardiolipin loss and membrane depolarization in rat brain mitochondria

Oxidative stress induced by Fe2+ (50 microM) and ascorbate (2 mM) in isolated rat brain mitochondria incubated in vitro leads to an enhanced lipid peroxidation, cardiolipin loss and an increased formation of protein carbonyls. These changes are associated with a loss of mitochondrial membrane potential (depolarization) and an impaired activity of electron transport chain (ETC) as measured by MTT reduction assay. Butylated hydroxytoluene (0.2 mM), an inhibitor of lipid peroxidation, can prevent significantly the loss of cardiolipin, the increased protein carbonyl formation and the decrease in mitochondrial membrane potential induced by Fe2+ and ascorbate, implying that the changes are secondary to membrane lipid peroxidation. However, iron-ascorbate induced impairment of mitochondrial ETC activity is apparently independent of lipid peroxidation process. The structural and functional derangement of mitochondria induced by oxidative stress as reported here may have implications in neuronal damage associated with brain aging and neurodegenerative disorders.     

Inhibitory effect of the flavonoid silymarin on the erythrocyte hemolysis induced by phenylhydrazine

The flavonoid silymarin, which is used as a therapeutical agent in the treatment of liver diseases, can inhibit the hemolysis and lipid peroxidation induced by phenylhydrazine on erythrocytes obtained from rats treated with the flavonoid. This effect is ascribed to the antioxidant properties as a free radical scavenger exhibited by the flavonoid. Silymarin failed to inhibit the glutathione depletion induced by phenylhydrazine on erythrocytes. It is proposed that the flavonoid acts at the membrane level of the cell avoiding the lipid peroxidative and fluidizing effect of phenylhydrazine.     

The in vivo toxicity of carbon tetrachloride and carrageenan on heart microsomes: analysis by Fourier transform infrared spectroscopy

We investigated the sensitivity of rat heart microsomes to free radical attack using Fourier transform infrared (FT-IR) spectroscopy. This physico-chemical method seemed a valuable technique: quite sensitive to changes in the vibrational spectra. The spectral variations observed between normal and treated rats were in great part due to reactive oxygen species that led to changes in protein conformation involving beta-sheets, aggregation of proteins, and modification of protein synthesis. Carrageenan-induced inflammation slightly enhanced the total lipid content; rearrangement of acyl chains and accumulation of cholesterol esters and phospholipids also occurred in the treated rats. Carbon tetrachloride induced a decrease in both lipid and protein contents. The level of glucidic substrates was diminished with carbon tetrachloride and enhanced with carrageenan; these changes were due to metabolic interactions between cell components and drugs. FT-IR spectroscopy provided an accurate means to monitor, in rat heart, the in vivo effects of inflammatory and peroxidative damages, to discriminate and classify the affected cells, and to correlate the findings with known physiological and biochemical data in close relationship with metabolic disruptions induced by the two xenobiotics.     

Nanocapsulated curcumin: oral chemopreventive formulation against diethylnitrosamine induced hepatocellular carcinoma in rat

Toxic outcome of chemical therapeutics as well as multidrug resistance are two serious phenomena for their inacceptance in cancer chemotherapy. Antioxidants like curcumin (Cur) have gained immense importance for their excellent anticarcinogenic activities and minimum toxic manifestations in biological system. However, Cur is lipophilic and thus following oral administration hardly appears in blood indicating its potential therapeutic challenge in cancer therapy. Nanocapsulated Cur has been used as a drug delivery vector to focus the effectiveness of these vesicles against hepatocellular carcinoma. The theme of work was to evaluate effectiveness in oral route of polylactide co-glycolide (PLGA) Nanocapsulated curcumin (Nano Cur) against diethylnitrosamine (DEN) induced hepatocellular carcinoma (HCC) in rat. Nano Cur of average diameter 14nm and encapsulation efficiency of 78% were prepared. Fourier Transform Infra Red (FTIR) analysis revealed that there is no chemical interaction between drug and the polymer. Three i.p. injections of the chemical hepatocarcinogen DEN at 15days interval causes hepatotoxicity, the generation of reactive oxygen species (ROS), lipid peroxidation, decrease in plasma membrane microviscosity and depletion of antioxidant enzyme levels in liver. Nano Cur (weekly oral treatment for 16weeks at 20mg/kg b.wt) in DEN induced HCC rats exerted significant protection against HCC and restored redox homeostasis in liver cells. Nanocapsulated Cur caused cancer cell apoptosis as visualized by ApoBrdU analysis. Histopathological analysis confirmed the pathological improvement in the liver. Nano Cur was found to be a potential formulation in oral route in combating the oxidative damage of hepatic cells and eliminating DEN induced hepatocellular cancer cells in rat whereas identical amount of free Cur treatment was found almost ineffective.     

Alcohol and thermally oxidized pufa induced oxidative stress: role of N-acetyl cysteine

Alcohol related disabilities are one of the world's major public health concerns. The effects of alcohol intake include alteration of redox state, acetaldehyde and free radical production, which lead to membrane damage. The damage caused by alcohol is enhanced by polyunsaturated fatty acid ingestion. When alcohol is taken along with thermally oxidized sunflower oil, the toxicity is still more pronounced due to toxic metabolites produced during heating. In our study, we have analysed the effects of a thiol supplier N-acetyl cysteine on alcohol, thermally oxidized sunflower oil and alcohol + thermally oxidized sunflower oil induced toxic effects in male Wistar rats. The activities of liver marker enzymes (alkaline phosphatase and gamma-glutamyl transferase), triglycerides in plasma and lipid peroxidative indices (thiobarbituric acid reactive substances and hydroperoxides) were increased in these groups when compared to normal, which were brought down in N-acetyl cysteine treated groups. The antioxidant status (Superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase) was decreased in tissues of these groups, which were found to be improved in N-acetyl cysteine treated groups. Thus our results show that N-acetyl cysteine regresses the oxidative damage induced by Alcohol, thermally oxidized sunflower oil and alcohol + thermally oxidized sunflower oil.     

Changes in tissue defence system in white spot syndrome virus (WSSV) infected Penaeus monodon

The present study examined the changes occurring in the pro phenoloxidase system and antioxidant defence status in haemolymph, hepatopancreas and muscle tissue of white spot syndrome virus (WSSV) infected Penaeus monodon. Tiger shrimps (P. monodon) were infected with white spot virus by intramuscular injection of the virus inoculum. Levels of lipid peroxides and the activities of phenoloxidase, glutathione-dependent antioxidant enzymes [glutathione peroxidase (GPX), glutathione-S-transferase (GST)] and antiperoxidative enzymes [superoxide dismutase (SOD) and catalase (CAT)] were determined. WSSV infection induced a significant increase in lipid peroxidation in haemolymph, muscle and hepatopancreas of experimental P. monodon compared to normal controls. This was paralleled by significant reduction in the activities of phenol oxidase, glutathione-dependent antioxidant enzymes and antiperoxidative enzymes. The results of the present study indicate that the tissue antioxidant defence system in WSSV infected P. monodon is operating at a lower rate, which ultimately resulted in the failure of counteraction of free radicals, leading to oxidative stress as evidenced by the increased level of lipid peroxidation.