Effect of aliphatic aldehydes on the lipid peroxidation and chemiluminescence of biological systems under oxidative stress

The effect of several aliphatic aldehydes on lipid peroxidation was evaluated by measuring the oxygen uptake rate, thiobarbituric acid-reactive products formation and the emitted visible chemiluminescence intensity. Measurements were carried out in brain homogenates and erythrocyte plasma membrane and liver microsomal fractions. In all systems studied, aldehydes (25 mmol/L) (e.g. acetaldehyde, 2,2-dimethylpropanal), increased the intensity of the luminescence associated with the oxidation process. In contrast, aldehyde incorporation decreased TBARS production and the rate of oxygen uptake. The increased luminescence intensity is explained in terms of secondary reactions of aldehyde derived free radicals. These results clearly indicate that extreme care must be exercized in the intepretation of chemiluminescence data in the presence of aldehydes. © 1997 John Wiley & Sons, Ltd.     

Early lipoic acid intake protects retina of diabetic mice

The aim of this study was to test the effect of lipoic acid treatment on the retina after a short diabetic insult. Diabetes was induced by alloxan and mice were divided into sub-groups; control, diabetic, diabetic+insulin and all groups received±lipoic acid (100 mg/kg body weight) for 3 weeks. GSH content, MDA concentration, GPx activity were measured and electroretinograms (ERG) were recorded. Early administration of lipoic acid to diabetic mice prevented the statistically significant decreases of GSH content and GPx activity and normalized MDA concentration. Moreover, lipoic acid restored electroretinogram b-wave amplitude of diabetic animals to control values. Lipoic acid has a protective effect on the diabetic retina.     

α-亚麻酸对糖尿病大鼠炎症介质和氧化应激的影响

目的:观察α-亚麻酸(ALA)对糖尿病大鼠体内炎症介质和氧化应激的影响,探讨ALA在糖尿病防治中的作用。方法:雄性SD大鼠高脂饮食喂养4周后,腹腔注射链脲佐菌素(STZ)30 mg/kg建立2型糖尿病(T2DM)模型。将大鼠随机分为3组(n=10):正常对照组、糖尿病模型组和ALA治疗组(500μg/kg.d)。4周后测定大鼠血清中肿瘤坏死因子(TNF-α)、可溶性P-选择素(sP-selectin)、可溶性细胞间黏附分子(sICAM-1)、一氧化氮(NO)、丙二醛(MDA)的含量以及超氧化物岐化酶(SOD)和过氧化氢酶(CAT)的活性。结果:与正常对照组相比,糖尿病大鼠血清中炎症介质TNF-α、sP-selectin和sICAM-1的含量增加,血清NO含量下降而MDA升高,同时抗氧化酶SOD和CAT的活性降低;ALA治疗可显著降低糖尿病大鼠血清中TNF-α、sP-selectin和sICAM-1的含量(与STZ+vehicle组相比,P<0.01),增加血清NO水平并减少MDA含量,升高抗氧化酶SOD和CAT的活性(与STZ+vehicle组相比,均P<0.05)。结论:ALA可显著降低糖尿病大鼠血清炎症介质的生成,减轻氧化应激水平,具有抗炎和抗氧化作用。提示ALA对糖尿病及糖尿病并发症的发生发展可能具有一定的防治作用。     

Effect of oral methionine on blood lipid peroxidation and antioxidants in alloxan-induced diabetic rats

Supplementation of thiol compounds has been suggested to protect against the toxic effects of reduced oxygen species by contributing to the thiol pool of the cell. The present study was designed to determine whether supplementation of methionine in the diet of diabetic animals protected against the oxidative stress in diabetic pathology. Oral methionine was administered at a dosage of 330 mg/100 g feed to diabetic rats. The effect was compared with the effect of insulin administration. Levels of lipid peroxides were measured in plasma, erythrocytes, and erythrocyte membrane. Anti-oxidants were measured in plasma. Diabetic condition was associated with increased lipid peroxidation and depletion in antioxidant levels. Although methionine did not affect the level of blood glucose and some of the antioxidants, it lowered the lipid peroxide content in blood. Erythrocyte lipid peroxidation activity was unaffected by methionine treatment. Administration of insulin lowered both plasma and erythrocyte lipid peroxide levels.     

Effect of salt stress on antioxidant defense systems,lipid peroxidation,and chlorophyll content in green bean

Salt stress-induced changes in antioxidant enzymes, such as catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase (GR), total chlorophyll content, and lipid peroxidation measured as malondialdehyde (MDA) content, in leaves of a green bean genotype Gevas sirsk 57 (GS57) and cv. Fransiz 4F-89 differing in salt tolerance were investigated. Plants were subjected to three salt treatments (0, 50, and 100 mM NaCl) under controlled climatic conditions for 7 days. The salt-sensitive cv. 4F-89 exhibited a decrease in GR activity at all salt treatments, but the salt-tolerant genotype GS57 showed only a slight decrease in GR under 50 mM salt treatment and an increase under 100 mM salt treatment. CAT and APX activities increased with increasing salt stress in both varieties. CAT and APX activities were higher in the salt-tolerant GS57 than salt-ensitive cv. 4F-89. The two varieties showed an increase in MDA content with an increase in salinity, but the increase in sensitive cv. 4F-89 under salt stress was higher than that in salt-tolerant GS57 genotype. The increasing NaCl concentration caused a reduction in the chlorophyll content in cv. 4F-89 but not in GS57.     

Protective effect of lipoic acid on adriamycin induced lipid peroxidation in rat kidney

Adriamycin, which is widely used in the treatment of various neoplastic conditions, exerts toxic effects in many organs. The present study was designed to investigate the effect of lipoic acid upon adriamycin induced peroxidative damages in rat kidney. The increase in peroxidated lipids on adriamycin administration was accompanied by alterations in the antioxidant defense systems. The extent of nephrotoxicity induced by adriamycin was evident from the decreased activities of the enzymes -glutamyl transferase and -glucuronidase in the rat renal tissues. The study was carried out with adult male albino rats of Wistar strain, which comprised of one control and three experimental groups. Group I rats served as controls. GroupII rats received adriamycin (1 mg kg^–1 body wt day^–1) intravenously through the tail vein. Group III rats were given lipoic acid (35 mg kg^–1 body wt day^–1) intraperitoneally. Group IV rats were given lipoic acid 24 h before the administration of adriamycin. Rats subjected to adriamycin administration showed a decline in the thiol capacity of the cell accompanied by high malondialdehyde levels along with lowered activities of catalase, superoxide dismutase, glutathione peroxidase and glutathione metabolizing enzymes (glutathione reductase, glucose-6-phosphate dehydrogenase, glutathione-S-transferase). Lipoic acid pretreatment also restored the activities of -glutamyl transferase and -glucuronidase nearly to control levels thereby suggesting nephroprotection. The study has highlighted the beneficial effects of lipoic acid pretreatment in reversing the damages caused by adriamycin and thereby bringing about an improvement in the oxidative stress parameters.     

Ascorbic acid prevents lipid peroxidation and oxidative damage of proteins in guinea pig extrahepatic tissue microsomes

It has recently been indicated that in the absence of free iron, NADPH initiates oxidative damage of proteins in guinea pig liver microsomes and also lipid peroxidation and protein damage in cardiac microsomes and that ascorbic acid specifically inhibits both the lipid peroxidation and protein damage [Mukhopadhyay CK, Chatterjee IB: J Biol Chem 269: 13390–13397, 1994; Mukhopadhyay Met al.: Mol Cell Biochem 126: 69–75, 1993]. In this paper we demonstrate that Fe(III)-independent NADPH-initiated lipid peroxidation and oxidative damage of proteins occur in the microsomes of all the extrahepatic tissues including lung, kidney, adrenal gland and brain and that both the lipid peroxidation and protein damage are specifically prevented by ascorbic acid. We further demonstrate that when NADPH is replaced by as the electron donor, the lipid peroxidation and protein damage are also inhibited by ascorbic acid.Abbreviations AH₂ ascorbic acid - SOD bovine erythrocyte superoxide dismutase - GSH glutathione - XOD xanthine oxidase - cyt P450 cytochrome P450 - DFO desferrioxamine     

Effects of high-fat,low-cholesterol diets on hepatic lipid peroxidation and antioxidants in apolipoprotein E-deficient mice

The present study describes the effects of several high-fat low-cholesterol antiatherogenic diets on the hepatic lipid peroxidation and hepatic antioxidant systems in apolipoprotein E-deficient mice. Eighty mice were distributed into five groups and fed with regular mouse chow or chow supplemented with coconut, palm, olive and sunflower seed oils. After ten weeks, they were sacrificed and the livers were removed so that lipid peroxidation and -tocopherol concentrations, and superoxide dismutase, glutathione peroxidase and glutathione reductase activities could be measured. The size of the atherosclerotic lesions in the aortas was also measured. Results showed that the diets supplemented with olive oil, palm oil or sunflower seed oil significantly decreased the size of the lesion. However, there was an association between those mice that were on diets supplemented with palm or coconut oils and a significant increase in hepatic lipid peroxidation. This association was not found in animals fed with olive or sunflower seed oils, the diets with the highest content of vitamin E. The dietary content of vitamin E was significantly correlated (r = 0.98; p < 0.05) with the hepatic concentration of this compound. Our study suggests that the high content of vitamin E in olive oil or sunflower seed oil may protect from the undesirable hepatotoxic effects of high-fat diets in apo E-deficient mice and that this should be taken into account when these diets are used to prevent atherosclerosis.     

Effect of laser pretreatment on germination and membrane lipid peroxidation of Chinese pine seeds under drought stress

The germination of laser-irradiated Chinese pine seeds was carried out under drought stress.The activities of superoxide dismutase (SOD) and peroxidase (POD),and the content of malondialdehyde (MDA) were determined.Results showed notably increased germination percentage,root length,vitality index and fresh weight.The SOD and POD protective enzyme system activity of the Chinese pine seedlings obviously rose.It can be concluded that the germination and juvenile resistance of Chinese pine seeds under drought stress are enhanced after laser processing.     

Effect of laser pretreatment on germination and membrane lipid peroxidation of Chinese pine seeds under drought stress

The germination of laser-irradiated Chinese pine seeds was carried out under drought stress. The activities of superoxide dismutase (SOD) and peroxidase (POD), and the content of malondialdehyde (MDA) were determined. Results showed notably increased germination percentage, root length, vitality index and fresh weight. The SOD and POD protective enzyme system activity of the Chinese pine seedlings obviously rose. It can be concluded that the germination and juvenile resistance of Chinese pine seeds under drought stress are enhanced after laser processing. Translated from Journal of Shaanxi Normal University (Natural Science Edition), 2006, 34(2): 40–43 [译自: 陕西师范大学学报 (自然科学版)]     

干旱胁迫下外源水杨酸对黄瓜幼苗膜脂过氧化和光合特性的影响

为了探讨外源水杨酸(SA)提高植物抗旱性的相关机制,研究了干旱胁迫下(基质含水量为饱和持水量的60％和50％),根际施用外源SA对黄瓜幼苗生长、膜脂过氧化、脯氨酸积累、水分利用效率、净光合速率(Pn)和叶绿素荧光参数的影响.结果表明:SA处理能够缓解干旱胁迫对黄瓜幼苗生长、Pn和水分利用效率的抑制,减小膜脂过氧化程度,促进脯氨酸的积累;添加外源SA显著减小了干旱胁迫下黄瓜幼苗的PSⅡ最大光化学效率、PSⅡ实际光化学效率、PSⅡ潜在活性、PSⅡ有效光化学效率和光化学猝灭系数的下降幅度,抑制了非光化学猝灭系数的升高.添加外源SA可以缓解干旱胁迫造成的膜脂过氧化对膜系统的氧化损伤,并通过增强PSⅡ反应中心活性提高了Pn,有助于水分的利用,同时增大渗透调节能力,减少水分的散失,提高水分利用效率,从而增强植株对干旱的适应能力.     

The role of dietary copper,manganese, selenium,and vitamin E in lipid peroxidation in tissues of the rat

The role of dietary Cu and Mn in maintaining tissue integrity, through the effects of these metals on activity of the superoxide dismutase (SOD) enzyme, and their interactions in peroxidative pathways involving Se and vitamin E was investigated. Weanling rats were fed diets deficient in Mn, Cu, Se, and/or vitamin E for 35 days, in a factorial experimental design. Dietary effects on peroxidation, measured in mitochondrial fractions prepared from liver and heart tissue, were compared with changes in the activities of glutathione peroxidase and the Cu and MnSOD enzymes. Decreased heart MnSOD and CuSOD activities, resulting from dietary Mn and Cu deficiencies, were both associated with increased peroxidation. Adequate Se (and glutathione peroxidase activity) prevented the peroxidation associated with either of these deficiencies, but was ineffective with a combined Cu−Mn deficiency. These effects of Se were only observed in tissue lacking glutathione transferase activity. Effects of Cu, Mn, and Se on peroxidation appeared to be present at both levels of vitamin E, although in both tissues, vitamin E deficiency greatly increased the overall peroxidation. Comparison of these in vitro peroxidation results with the deficiency associated lesions observed in vivo indicates that changes in SOD activities and peroxidation pathways may be the dominant cause of these lesions in only some cases. In others, the roles of Cu and Mn in different metabolic pathways appear to be of greater importance.     

Eicosanoid production in experimental alcoholic liver disease is related to vitamin E levels and lipid peroxidation

We investigated the association between vitamin E, lipid peroxidation and eicosanoid production in experimental alcoholic liver injury. We used the intragastric feeding rat model in which animals were fed corn oil and ethanol (CO+E) and corn oil and dextrose (CO+D) for 2 and 4 week periods. At sacrifice, we measured plasma levels of alpha-tocopherol, 8-isoprostane, thromboxane B₂(TXB₂) and 6-ketoprostaglandin F₁(6-KetoPGF₁). Animals fed CO+E had significantly lower concentrations of -tocopherol and higher concentrations of 8 isoprostane at both 2 and 4 weeks. a significant inverse correlation was seen between -tocopherol concentrations and the TXB₂: PGF₁ ratio (r=0.72, p<0.01). A positive correlation was seen between the TXB₂: PGF₁ ratio and 8 isoprostane levels (r=0.84, p<0.001). These results suggest that vitamin E depletion and enhanced lipid peroxidation may affect eicosanoid metabolism in experimental alcoholic liver disease in such a way so as to increase the thromboxane to prostacyclin ration.Abbreviations PGH₂ Prostaglandin H₂ - PGL₂ Prostacyclin - CO+E Corn Oil and Ethanol - CO+D Corn Oil and Dextrose - TXB₂ Thromboxane B₂ - TXA₂ Thromboxane A₂     

Alpha-lipoic acid affects the oxidative stress in various brain structures in mice with methionine and choline deficiency

Deficiency in methionine or choline can induce oxidative stress in various organs such as liver, kidney, heart, and brain. This study was to examine the effects of alpha-lipoic acid (LA) on oxidative stress induced by methionine and choline deficiency (MCD) in several brain structures. Male mice C57BL/6 (n = 28) were divided into four groups: (1) control – continuously fed with standard chow; (2) LA – fed with standard chow and receiving LA; (3) MCD2 – fed with MCD diet for two weeks, and (4) MCD2+LA – fed with MCD diet for two weeks and receiving LA (100 mg/kg/day intraperitonealy [i.p.]). Brain tissue (cortex, hypothalamus, striatum and hippocampus) was taken for determination of oxidative stress parameters. MCD diet induced a significant increase in malondialdehyde and NOx concentration in all brain regions, while LA restored their content to normal values. Similar to this, in MCD2 group, activity of total SOD, MnSOD, and Cu/ZnSOD was reduced by MCD diet, while LA treatment improved their activities in all brain structures. Besides, in MCD2 group a decrease in catalase activity in cortex and GSH content in hypothalamus was evident, while LA treatment induced an increase in catalase activity in cortex and striatum and GSH content in hypothalamus. LA treatment can significantly reduce lipid peroxidation and nitrosative stress, caused by MCD diet, in all brain regions by restoring antioxidant enzymes activities, predominantly total SOD, MnSOD, and Cu/ZnSOD, and to a lesser extent by modulating catalase activity and GSH content. LA supplementation may be used in order to prevent brain oxidative injury induced by methionine and choline deficiency.     

Walker-256 tumor growth causes oxidative stress in rat brain

The elevated rate of oxygen consumption and high amount of polyunsaturated fatty acids make the central nervous system vulnerable to oxidative stress. The effect of Walker-256 tumor growth on oxi-reduction indexes in the hypothalamus (HT), cortex (CT), hippocampus (HC) and cerebellum (CB) of male Wistar rats was investigated. The presence of the tumor caused an increase in thiobarbituric acid reactant substances (TBARs) in the HT, CB and HC. Due to tumor growth, the activity of glucose-6-phosphate dehydrogenase increased in the HT and CB, whereas citrate synthase activity was reduced in the HT, CT and CB. Therefore, the potential for generation of reducing power is increased in the cytosol and decreased in the mitochondria of various brain regions of Walker-256 tumor-bearing rats. These changes occurred concomitantly with an unbalance in the brain enzymatic antioxidant system. The tumor decreased the activities of catalase in the HT and CB and of glutathione peroxidase in the HT, CB and HC, and raised the CuZn-superoxide dismutase activity in the HT, CB and HC. These combined findings indicate that Walker-256 tumor growth causes oxidative stress in the brain.     

Antioxidant effect of conjugated linoleic acid and vitamin A during non enzymatic lipid peroxidation of rat liver microsomes and mitochondria

In the study reported here the effect of conjugated linoleic acid (CLA) and vitamin A on the polyunsaturated fatty acid composition, chemiluminescence and peroxidizability index of microsomes and mitochondria isolated from rat liver was analyzed. The effect of CLA on the polyunsaturated fatty acid composition of native microsomes was evidenced by an statistically significant p < 0.007 decrease of linoleic acid C18:2 n6, whereas in mitochondria it was observed a decrease p < 0.0001 of arachidonic acid C20:4 n6 when compared with vitamin A and control groups. Docosahexaenoic acid C22:6 n3 in mitochondria was reduced p < 0.04 in CLA and vitamin A groups when compared with control. After incubation of microsomes or mitochondria in an ascorbate (0.4 mM)-Fe⁺⁺ (2.15 M) system (120 min at 37°C) it was observed that the total cpm/mg protein originated from light emission: chemiluminescence was lower in liver microsomes or mitochondria obtained from CLA group (received orally: 12.5 mg/daily during 10 days) than in the vitamin A group (received intraperitoneal injection: daily 0.195 g/kg during 10 days). CLA reduced significantly maximal induced chemiluminescence in microsomes relative to vitamin A and control groups, whereas in mitochondria the effect was observed relative to control group The polyunsaturated fatty acid composition of liver microsomes or mitochondria changed by CLA and vitamin A treatment. The polyunsaturated fatty acids mainly affected when microsomes native and peroxidized from control group were compared were linoleic, linolenic and arachidonic acids, while in vitamin A group linoleic and arachidonic acid were mainly peroxidized, whereas in CLA group only arachidonic acid was altered. In mitochondria obtained from the three groups arachidonic acid and docosahexaenoic acid showed a significant decrease when native and peroxidized groups were compared. As a consequence the peroxidizability index, a parameter based on the maximal rate of oxidation of fatty acids, show significant changes in the CLA group compare vitamin A and control groups. The simultaneous analysis of peroxidizability index, chemiluminescence and fatty acid composition demonstrated that CLA is more effective than vitamin A protecting microsomes or mitochondria from peroxidative damage.     

Effect of physical restraint on oxidative stress in mice fed a selenium and vitamin E deficient diet

Physical restraint has been associated with increased oxidative damage to lipid, protein, and DNA. The purpose of this experiment was to determine whether physical restraint would further exacerbate oxidative stress in mice fed a selenium (Se) and vitamin E (VE) deficient diet. Three-week-old mice were fed a Torula yeast diet containing adequate or deficient Se and VE. Menhaden oil was added to the deficient diet to impose an additional oxidative stress. After 4 wk feeding, half the mice in each group were restrained for 5 d in well-ventilated conical tubes for 8 h daily. Mice fed the Se and VE deficient diets had increased liver thiobarbituric acid-reactive substance (TBARS) levels and decreased liver glutathione peroxidase (GPX1) activity and α-tocopherol levels. Plasma corticosterone levels were elevated in restrained mice fed the deficient diet compared to unrestrained mice fed the adequate diet. Restraint had no effect on liver TBARS or α-tocopherol levels. Liver GPX1 activity, however, was lower in restrained mice fed the adequate diet. In addition, liver superoxide dismutase (SOD) activity was lower in the restrained mice fed the adequate or deficient diet. Thus, under our conditions, Se and VE deficient diet, but not restraint, increased lipid peroxidation in mice. Restraint, however, decreased antioxidant protection in mice due to decreased activities of GPX1 and SOD enzymes.     

Involvement of free radicals and oxidative stress in NAFLD/NASH

Abstract

Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease affecting high proportion of the population worldwide. NAFLD encompasses a large spectrum of conditions ranging from fatty liver to non-alcoholic steatohepatitis (NASH), which can progress to cirrhosis and cancer. NAFLD is considered as a multifactorial disease in relation to the pathogenic mechanisms. Oxidative stress has been implicated in the pathogenesis of NAFLD and NASH and the involvement of reactive oxygen species (ROS) has been suggested. Many studies show the association between the levels of lipid oxidation products and disease state. However, often neither oxidative stress nor ROS has been characterized, despite oxidative stress is mediated by multiple active species by different mechanisms and the same lipid oxidation products are produced by different active species. Further, the effects of various antioxidants have been assessed in human and animal studies, but the effects of drugs are determined by the type of active species, suggesting the importance of characterizing the active species involved. This review article is focused on the role of free radicals and free radical-mediated lipid peroxidation in the pathogenesis of NAFLD and NASH, taking characteristic features of free radical-mediated oxidation into consideration. The detailed analysis of lipid oxidation products shows the involvement of free radicals in the pathogenesis of NAFLD and NASH. Potential beneficial effects of antioxidants such as vitamin E are discussed.     

Local and systemic increase in lipid peroxidation after moderate experimental traumatic brain injury

Traumatic brain injury is a common event associated with neurological dysfunction. Oxidative damage, may contribute to some of these pathologic changes. We used a specific and sensitive marker of lipid peroxidation, the isoprostane 8,12-iso-iPF(2alpha) -VI, to investigate whether local and also systemic lipid peroxidation were induced following lateral fluid percussion (FP) brain injury in the rat. Animals were anesthetized and subjected to lateral FP brain injury of moderate severity, or to sham injury as controls. Urine was collected before anesthesia (baseline), 6 and 24 h after injury. Blood was collected at baseline, 1, 6 and 24 h after injury. Animals were killed 24 h after surgery and their brains removed for biochemical analysis. No significant difference was observed at baseline (preinjury) for urine and plasma 8,12-iso-iPF(2alpha) -VI levels between injured and sham-operated animals. By contrast, plasma and urinary levels increased significantly already at 1 and further increased 24 h following brain injury, when compared to sham-operated animals. Finally, compared with sham, injured animals had a significant increase in brain 8,12-iso-iPF(2alpha) -VI levels. These results demonstrate that moderate brain injury induces widespread brain lipid peroxidation, which is accompanied by a similar increase in urine and plasma. Peripheral measurement of 8,12-iso-iPF(2alpha) -VI levels after brain injury may be a reliable marker of brain oxidative damage.     

Antioxidant and oxidative stress changes in experimental cor pulmonale

Although right heart failure (RHF) contributes to 20% of all cardiovascular complications, most of the information available on RHF in general is based on the experiences with left heart failure. This study on RHF investigates changes in antioxidants and oxidative stress which are suggested to play a role in the transition from hypertrophy to failure. RHF subsequent to pulmonary hypertension was produced in rats by a single injection of monocrotaline (MCT, 60 mg/kg, i.p.). Based on hemodynamic, clinical and histopathologic observations, the animals were grouped in three functional stages at 1-, 2- and 6-week post-injection periods. In the 1-week group, RV pressure overload and hypertrophy, and a mild increase in antioxidant enzymes was seen. In the 2-week group, compensated HF, a significant increase in antioxidant enzymes, an increase in septal (IVS) wall thickness and leftward displacement of IVS without change in LV free wall were seen. In the 6-week group, lung and liver congestion, RVF and dilation, a decrease in antioxidant enzyme activities, increase in lipid peroxidation and severe bulging of the IVS into the left ventricle were seen. These changes in the hemodynamic, biochemical and histopathologic characteristics suggest that in early stages of MCT-induced pulmonary hypertension at 1 and 2 weeks, RV hypertrophy was accompanied by sustained hemodynamic function and an increase in antioxidant reserve. In the later stage at 6 weeks, clinical RHF was associated with abnormalities of the right heart systolic and diastolic function along with a decrease in antioxidant reserve. These biphasic changes in RV antioxidant enzymes, i.e. an increase during hypertrophy and a decrease in failure may suggest a role of oxidative stress in the pathogenesis of right ventricular dysfunction.