Antioxidant enzymes and lipid peroxides in children with cerebral palsy

Impaired antioxidant mechanisms are unable to inactivate free radicals that may induce a number of pathophysiological processes and result in cell injury. Thus, any abnormality in antioxidant defense systems could affect neurodevelopmental processes and could have an important role in the etiology of cerebral palsy (CP). The plasma levels of lipid peroxidation as plasma levels of malondialdehyde (MDA), activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) in plasma and erythrocytes were investigated in 34 CP children and compared with 61 normal controls. SOD, GPx and GR activities were spectrophotometrically assayed. Activities of SOD, GPx and GR in plasma did not differ significantly between CP children and the control group. Activities of erythrocyte GR in the CP patients were significantly lower compared with controls. MDA concentration did not differ statistically between the CP children and healthy subjects. In conclusion our results suggest that increased activities of erythrocyte GPx and decreased erythrocyte GR activities might be due to lesser physical activity of children with CP.     

Evaluation of Oxidative Stress in Autism: Defective Antioxidant Enzymes and Increased Lipid Peroxidation

Autism is a neurodevelopmental disorder of childhood with poorly understood etiology and pathology. This pilot study aims to evaluate the levels of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and levels of malondialdehyde (MDA), a marker of lipid peroxidation, in Egyptian autistic children. Autism is a neurodevelopmental disorder of childhood with poorly understood etiology and pathology. The present study included 20 children with autism diagnosed by DSM-IV-TR criteria and Childhood Autism Rating Scale. Controls included 25 age-matched healthy children. Cases were referred to Outpatient Clinic of Children with Special Needs Department, National Research Center, Cairo, Egypt. We compared levels of SOD, GSH-Px, and MDA in children with autism and controls. In children less than 6 years of age, levels of SOD, and GSH-Px were significantly lower in autistic children compared with their controls, while MDA was significantly higher among patients than controls. In children older than 6 years, there was no significant difference in any of these values between cases and controls. We concluded that children with autism are more vulnerable to oxidative stress in the form of increased lipid peroxidation and deficient antioxidant defense mechanism especially at younger children. We highlight that autistic children might benefit from antioxidants supplementation coupled with polyunsaturated fatty acids. Moreover, early assessment of antioxidant status would have better prognosis as it may decrease the oxidative stress before inducing more irreversible brain damage.     

Zinc Supplement Modulates Oxidative Stress and Antioxidant Values in Rats with Severe Acute Pancreatitis

Oxidative stress is a main factor in the pathogenesis of severe acute pancreatitis (SAP). The ability of zinc (Zn) to retard oxidative processes has been recognized for many years. This study aims to examine the levels of free oxygen radicals and antioxidant enzyme in SAP rats and know the effect of Zn supplementation on free oxygen radicals and antioxidant system in rats with SAP. Forty-five male Wistar rats were divided into three groups—the SAP group (n?=?15), the Zn-treated group (n?=?15), and the controlled group (n?=?15). For the SAP group, sodium taurocholate is injected into the pancreatic duct to induce SAP; for the Zn-treated group, Zn (5 mg/kg) is subcutaneously injected immediately after injection of 5 % sodium taurocholate. Firstly, the activity of erythrocyte glutathione peroxidase (GSH-Px), erythrocyte superoxide dismutase (SOD), and the content of plasma malondialdehyde (MDA), which are the toxic products of oxidative stress, is measured. Secondly, the levels of free oxygen radicals in the liver and kidney are detected. The result showed that the activity of GSH-Px and SOD was lower in the SAP group than that in the controlled group, although the content of plasma MDA increased. However, the activity of SOD and GSH-Px in the Zn-treated group was not significantly decreased after comparing with the controlled group; in the mean time, the content of MDA was not significantly increased either. Moreover, the content of free radical in liver and kidney was higher in the SAP group compared with the controlled group, but the content of free radical in the Zn-treated group was not higher than that in the controlled group (p?>?0.05). All of the above indicated that Zn may recover the activity of free radical-scavenging enzymes and decrease the content of free radical for the SAP group rats. In conclusion, the content of free radical increase may be one of the reasons that SAP rats are injured, and it is possible for Zn to be used to treat SAP through scavenging free radical and increasing the activity of SOD and GSH-Px of erythrocyte.     

The effect of melatonin against oxidative damage during total-body irradiation in rats

Melatonin has been reported to participate in the regulation of a number of important physiological and pathological processes. Melatonin, which is a powerful endogenous antioxidant, may play a role in the prevention of oxidative damage. The aim of this study was to investigate the effect of pretreatment with melatonin (5 mg kg(-1) and 10 mg kg(-1)) on gamma-radiation-induced oxidative damage in plasma and erythrocytes after total-body irradiation with a single dose of 5 Gy. Total-body irradiation resulted in a significant increase in plasma and erythrocyte MDA levels. Melatonin alone increased the levels of SOD and GSH-Px. Erythrocyte and plasma MDA levels in irradiated rats that were pretreated with melatonin (5 or 10 mg kg(-1)) were significantly lower than those in rats that were not pretreated. There was no significant difference between the effects of 5 and 10 mg kg(-1) on plasma MDA activities and CAT activities. However, erythrocyte MDA levels showed a dose-dependent decrease, while GSH-Px activities increased with dose. Our study suggests that melatonin administered prior to irradiation may protect against the damage produced by radiation by the up-regulation of antioxidant enzymes and by scavenging free radicals generated by ionizing radiation.     

The Role of Oxidative Stress in Amyotrophic Lateral Sclerosis and Parkinson’s Disease

We examined oxidative stress markers of 31 patients suffering from ALS, 24 patients suffering from PD and 30 healthy subjects were included. We determined the plasma levels of lipid peroxidation (malondialdehyde, MDA), of protein oxidative lesions (plasma glutathione, carbonyls and thiols) and the activity of antioxidant enzymes i.e. erythrocyte Cu,Zn-Superoxide dismutase (SOD), Glutathione peroxidase (GSH-Px) and catalase. MDA and thiols were significantly different in both neurodegenerative diseases versus control population. A trend for an enhancement of oxidized glutathione was noted in ALS patients. Univariate analysis showed that SOD activity was significantly decreased in ALS and GSH-Px activity was decreased in PD. After adjusting for demographic parameters and enzyme cofactors, we could emphasize a compensatory increase of SOD activity in PD. Different antioxidant systems were not involved in the same way in ALS and PD, suggesting that oxidative stress may be a cause rather than a consequence of the neuronal death.     

Do Zinc and Selenium Prevent the Antioxidant, Hepatic and Renal System Impairment Caused by Aspirin in Rats?

Aspirin is widely used as an antiinflammatory drug especially in children with rheumatic fever arthritis. The diminishing effects of aspirin on antioxidant enzymes and hepato-renal systems at high doses are well-known. It is now evident that the damage at antioxidant system worsens the clinical picture of the disease and prolongs the treatment time. Thus, we investigated the effect of antioxidant enzyme cofactors-zinc and selenium-supplementation on superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels (erythrocyte and liver) and hepato-renal toxicity during aspirin treatment at therapeutic doses. The rats were divided into five groups. The first and second groups were given aspirin 75 mg/kg/day and aspirin plus selenium (Selenium 200, selenium 200 mg tablet as selenium yeast, GNC) and zinc (Zinc 100, zinc 100 mg tablet as zinc gluconate, GNC), respectively, the third and fourth take 50 mg/kg/day aspirin and aspirin plus selenium and zinc twice a day, respectively. The fifth group was control. The rats were treated with aspirin for 5 weeks as in the treatment of rheumatic fever arthritis in children. Erythrocyte SOD and MDA levels were preserved with supplementation, whereas there was no change for GSH-Px levels. Liver SOD, GSH-Px, and MDA levels were not changed. In zinc- and selenium-supplemented groups, the levels of serum alanine aminotransferase, uric acid, and direct bilirubin levels were found statistically decreased compared with nonsupplemented groups. There was no significant histopathologic change in specimens of hepatic and renal tissues. Trace element supplementation may prevent free radical damage and shorten treatment time in children using long-term aspirin treatment.     

Effects of garlic extract consumption on plasma and erythrocyte antioxidant parameters in atherosclerotic patients

Effects of ingesting garlic extract on plasma and erythrocyte antioxidant parameters of atherosclerotic patients were investigated in this study. Eleven patients with atherosclerosis participated in the study. They ingested a dose of 1 ml/kg body weight of garlic extract daily for 6 months (study period). Before and after this period, fasting blood samples were obtained, and oxidant (malondialdehyde, MDA and xanthine oxidase, XO) and antioxidant (superoxide dismutase, SOD and glutathione peroxidase, GSH-Px) parameters were studied in plasma and erythrocytes obtained from the patients. Blood samples obtained from 11 healthy subjects served as the controls. Plasma XO activity and MDA levels were higher, but plasma and erythrocyte GSH-Px activities were lower, in patients with atherosclerosis relative to those of the control group. Our results showed that ingestion of garlic extract leads to significantly lowered plasma and erythrocyte MDA levels in the patients even in the absence of changes in antioxidant enzyme activities. Our results also demonstrated the presence of oxidant stress in blood samples from patients with atherosclerosis, but ingesting garlic extract prevented oxidation reactions by eliminating this oxidant stress. Thus, it is possible that reduced peroxidation processes may play a part in some of the beneficial effects of garlic in atherosclerotic diseases.     

Plasma and erythrocytes antioxidant status and trace element levels in proteinuric patients with moderate glomerular function.

The objective of the study was to investigate the effect of moderate glomerular dysfunction on oxidative stress. We determined the plasma and erythrocyte malondialdehyde (MDA) levels, as a marker of lipid peroxidation, erythrocyte glutathione (GSH) levels and activities of GSH-Px, GSH Red and SOD as an antioxidant enzymes, and plasma trace element levels containing Fe, Cu and Zn in twenty proteinuric patients (6.8 +/- 5.1 g/day) with moderate glomerular function and in 20 anemic control subjects. We found that the erythrocyte and plasma MDA levels and erythrocyte GSH-Px activities were significantly higher (p < 0.001, p < 0.001, p < 0.001, respectively) and the erythrocyte GSH levels and activities of GSH-Red and SOD activities were significantly lower (p < 0.001, p < 0.001, p < 0.001, respectively) in the patients than in the anemic subjects. Plasma Fe and Zn levels were not to be found significantly different in the patients compared to the anemic subjects. But plasma Cu levels were significantly higher in the patients (p < 0.05) when compared with the levels of anemic subjects. This study was concluded that cellular antioxidant activity decreases in proteinuric patients with moderate glomerular function. This may increase lipid peroxidation reactions by causing oxidative stress in erythrocyte membranes.     

Association between dietary fat and antioxidant status of Tunisian type 2 diabetic patients

BACKGROUND: The antioxidant enzymes: superoxide dismutase (Cu/Zn SOD) and glutathione peroxidase (GSH-Px) provide a defense against the damage of cells by reactive oxygen species, which increased in diabetic state. It was demonstrated that dietary treatment could improve the antioxidant status in patients with type 2 diabetes mellitus. This study was undertaken to determine if erythrocyte Cu/Zn SOD and GSH-Px activities correlate with dietary nutrients in 35 selected type 2 diabetic patients (21 women and 14 men) without diabetic complications. RESULTS: We found that erythrocyte Cu/Zn SOD was diminished in patients with poor controlled diabetes and GSH-Px activity was significantly decreased in obese compared with non-obese type 2 diabetic patients (1.07+/-0.87 and 2.36+/-1.99 U/ml, respectively; P=0.024). Both erythrocyte Cu/Zn SOD and GSH-Px activities were positively correlated to erythrocyte omega3-polyunsaturated fatty acids (PUFA). In non-obese diabetic patients, only GSH-Px activity was correlated negatively to the fraction of linoleic acid (18:2omega6) and arachidonic acid (20:4omega6) in erythrocytes phospholipids. CONCLUSIONS: The data of this study reveal that activities of erythrocyte antioxidant enzymes were altered in type 2 diabetic patients. Further studies are needed to determine if diet supplemented with omega3-PUFA is required to improve antioxidant defense system in diabetic state.     

Osteoblast cytoskeletal modulation in response to compressive stress at physiological levels

In this study we assessed activities of antioxidant enzymes, lipid peroxidation end-products, and nitric oxide (NO) levels in women with postmenopausal osteoporosis (PMO). Relationship between oxidative stress parameters and NO levels with bone mineral density (BMD) and clinical variables influencing bone mass and health related quality of life measures was also investigated in women with PMO. Postmenopausal women (n = 87), aged 40–65, without previous diagnosis or treatment for osteoporosis and independent in daily living activities were included. BMD was measured at the lumbar spine and proximal femur using dual-X-ray absorptiometry (DXA). Erythrocyte catalase (CATe) enzyme activity, erythrocyte and plasma enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and lipid peroxidation end-product malondialdehyde (MDA) and nitrite/nitrate levels, by product of NO were studied. A total of 23 healthy non-porotic women were included as controls. Women with PMO had significantly lower erythrocyte CATe enzyme activity and higher erythrocyte malondialdehyde (MDAe) and erythrocyte nitric oxide (NOe) levels in comparison to controls whereas erythrocyte SODe and GSH-Px enzyme activity was similar. In plasma, osteporotic women had significantly higher SOD enzyme activity and higher MDA levels whereas similar GSH-Px enzyme activity and NO levels compared to non-porotic controls. Significant correlation was found between erythrocyte SODe, CATe enzyme activity and NOe levels with proximal femur BMD. Some of the quality of life scores as pain, mental, and social functions correlated with antioxidant enzyme activities and NO levels. Consequently, oxidative stress markers may be an important indicator for bone loss in postmenopausal women. Further researches assessing the oxidative stress markers and NO in bone tissue and changes with anti-osteoporotic drugs would be valuable to better understand the role of free radicals, antioxidants, and NO in the regulation of bone mass.     

Defective antioxidant defense system in patients with a human leptin gene mutation.

Antioxidant defense system prevents the organism from the detrimental effects of free radicals via scavenging or inhibiting their formation. Changes in the antioxidant defense mechanisms and alterations of several essential trace elements in both plasma and various tissues of ob/ob mice have been reported previously. Recent finding of the restoration of the defective antioxidant enzyme activity after leptin treatment in ob/ob mice suggests a putative role of leptin in modulation of antioxidant enzyme activity. Therefore, the aim of this study was to investigate whether antioxidant enzymes and trace elements could also be altered in patients with leptin gene mutation. Seven patients (five men and two women, two of them are homozygous and 5 are heterozygous) with leptin gene mutation and 31 healthy, sex- and age-matched and non-related to the patients (24 male and 9 female), control volunteers were enrolled in the study. Plasma and erythrocyte glutathione peroxidase (GSH-Px) and erythrocyte copper-zinc superoxide dismutase (CuZn-SOD) activities were measured spectrophotometrically. Plasma selenium (Se), manganese (Mn), zinc (Zn), copper (Cu), and iron (Fe) levels were measured by atomic absorption spectrophotometry. Mean Cu and Fe levels in patients were not significantly different than those in controls whereas mean Se, Zn and Mn levels were significantly lower in patients than those of controls (P=0.007, P=0.001, and P=0.001, respectively). Erythrocyte GSH-Px (39%), plasma GSH-Px (24%) and erythrocyte CuZn-SOD activities (32%) were significantly lower than those of the control group (P=0.001, P=0.002, P=0.001, respectively). In conclusion, our results demonstrate that the activity of antioxidant enzymes and plasma levels of Se, Zn and Mn levels were decreased in both homozygous and heterozygous subjects with leptin gene mutation. We suggest that both leptin and trace elements might be involved in the modulation of antioxidant defense system.     

Effects of halothane, enflurane, and isoflurane on plasma and erythrocyte antioxidant enzymes and trace elements

Alterations of the normal redox balance in mammals might be attributed to increases of plasma free-radical concentrations and/or a disruption of the protective mechanisms. These conditions lead to damage to cellular structure by the mechanism of lipoperoxidation, particularly in the liver, kidney, and central nervous system. In this study, the effect of general anesthesia on the oxidative metabolism of human plasma and erythrocytes was investigated. Forty-five patients undergoing anesthesia by using halothane, enflurane, or isoflurane were included in this study. Blood samples were taken preoperatively, the first hour, the first day, and the third day after the operation. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities and trace elements such as cofactor copper (Cu), zinc (Zn) and selenium (Se) levels were measured in plasma and red blood cells. Our results showed that halothane and enflurane administration increased the plasma GSH-Px activity and reduced zinc levels. In addition, they lowered SOD and GSH-Px activities and trace element levels on erythrocytes. Isoflurane had no effect on plasma antioxidant enzymes, but, similar to the other, isoflurane decreased the plasma zinc levels, erythrocyte SOD and GSH-Px activities and trace element levels. Gülhane Military Medical Academy     

Topiramate and Vitamin E Modulate the Electroencephalographic Records,Brain Microsomal and Blood Antioxidant Redox System in Pentylentetrazol-Induced Seizure of Rats

We investigated the effects of vitamin E and topiramate (TPM) administrations on pentylentetrazol (PTZ)–induced blood and brain toxicity in rats. Forty rats were randomly divided into five equal groups. The first and second groups were used for the control and PTZ groups, respectively. Fifty or 100 mg TPM were administered to rats constituting the third and fourth groups for 7 days, respectively. The TPM and vitamin E combination was given to animals in the fifth group. At the end of 7 days, all groups except the first received a single dose of PTZ. Blood and brain samples were taken at 3 hrs after PTZ administration. Lipid peroxidation levels of plasma, erythrocyte, brain cortex and brain microsomal fraction; nitric oxide levels of serum; and the number of spikes and epileptiform discharges of the EEG were increased by PTZ administration. Plasma and brain vitamin E concentration, erythrocyte glutathione peroxidase (GSH-Px) activity and latency to first spike of the EEG were decreased by PTZ. Plasma lipid peroxidation levels in the third group and plasma and erythrocyte lipid peroxidation levels in the fifth group were decreased compared to the second group, whereas brain vitamin C, vitamin E, erythrocyte GSH-Px and reduced glutathione (GSH) values increased in the fifth group. Brain microsomal GSH levels and EEG records in the third, fourth and fifth groups were restored by the TPM and vitamin E treatment. In conclusion, TPM and vitamin E seems to have protective effects on PTZ-induced blood and brain toxicity by inhibiting free radicals and supporting the antioxidant redox system.     

N-Acetylcysteine and Selenium Modulate Oxidative Stress,Antioxidant Vitamin and Cytokine Values in Traumatic Brain Injury-Induced Rats

It has been suggested that oxidative stress plays an important role in the pathophysiology of traumatic brain injury (TBI). N-acetylcysteine (NAC) and selenium (Se) display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties although there is no report on oxidative stress, antioxidant vitamin, interleukin-1 beta (IL)-1β and IL-4 levels in brain and blood of TBI-induced rats. We investigated effects of NAC and Se administration on physical injury-induced brain toxicity in rats. Thirty-six male Sprague–Dawley rats were equally divided into four groups. First and second groups were used as control and TBI groups, respectively. NAC and Se were administrated to rats constituting third and forth groups at 1, 24, 48 and 72 h after TBI induction, respectively. At the end of 72 h, plasma, erythrocytes and brain cortex samples were taken. TBI resulted in significant increase in brain cortex, erythrocytes and plasma lipid peroxidation, total oxidant status (TOS) in brain cortex, and plasma IL-1β values although brain cortex vitamin A, β-carotene, vitamin C, vitamin E, reduced glutathione (GSH) and total antioxidant status (TAS) values, and plasma vitamin E concentrations, plasma IL-4 level and brain cortex and erythrocyte glutathione peroxidase (GSH-Px) activities decreased by TBI. The lipid peroxidation and IL-1β values were decreased by NAC and Se treatments. Plasma IL-4, brain cortex GSH, TAS, vitamin C and vitamin E values were increased by NAC and Se treatments although the brain cortex vitamin A and erythrocyte GSH-Px values were increased through NAC only. In conclusion, NAC and Se caused protective effects on the TBI-induced oxidative brain injury and interleukin production by inhibiting free radical production, regulation of cytokine-dependent processes and supporting antioxidant redox system.     

Lipid peroxidation and scavenging enzyme levels in the liver of streptozotocin-induced diabetic rats

In this study, alterations in the liver antioxidant enzymes status and lipid peroxidation in short-term (8-weeks) and long-term (24-weeks) diabetic rats were examined. Glutathione peroxidase (GSH-Px) activity and malondialdehyde (MDA) levels were significantly increased, but superoxide dismutase (SOD) activity was significantly reduced in 8-weeks diabetic rats, compared to control. Catalase (CAT) activity, however, was found unchanged. In 24-weeks diabetic rats, while GSH-Px activity was unchanged, but SOD and CAT activities and MDA levels were significantly increased, compared to control. These results suggest that diabetes-induced alterations in tissue antioxidant system may reflect a generalized increase in tissue oxidative stress. It can be concluded that lipid peroxidation and antioxidant enzyme levels are elevated in diabetic condition. Hence, diabetes mellitus, if left untreated, may increase degenerative processes due to accumulation of oxidative free radicals.     

Oxidative stress in patients undergoing high-dose chemotherapy plus peripheral blood stem cell transplantation

Chemotherapy and radiation therapy are associated with increased formation of reactive oxygen species and depletion of critical plasma and tissue antioxidants. In patients undergoing high-dose chemotherapy, the plasma antioxidant concentration has been shown to decrease. However, these studies in which the oxidative stress status were investigated have a small number of patients and they are heterogeneous. In this study, the changes in certain trace elements together with oxidative stress parameters were investigated in 36 patients who had undergone autologous stem cell transplantation because of solid and hematological malignancies. Blood samples of the patients were examined before the high-dose chemotherapy (baseline), before stem cell transplantation (day -1), and after stem cell transplantation on day 1, 3, and 6. Erythrocyte zinc, silver, and iron levels were measured by atomic absorption spectrophotometry; malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were measured by UV-vis spectrophotometry. After high-dose chemotherapy, significant increases in the levels of MDA, GSH-Px, and SOD were observed. On the other hand, Cu levels remained the same while the levels of erythrocyte Zn and Fe were increased. Significant correlation was observed among MDA, GSH-Px, and SOD (p<0.05). High-dose chemotherapy gives rise to an increase in the oxidative stress and the reactive oxygen species. Standard parenteral nutrition protocols were found to be insufficient to lower this stress.     

Plasma values of oxidants and antioxidants in acute brain hemorrhage

The levels of oxidants xanthine oxidase (XO), nitric oxide (NO), and malondialdehyde (MDA) and of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GRD) were determined in plasma within 24 h after onset of hemorrhagic stroke in 17 patients (9 men and 8 women, aged 60.7+/-11.5 yr) and in 20 healthy controls (12 men and 8 women, aged 62.5+/-8.3 yr). Compared to controls, the plasma SOD and total superoxide scavenger activities (TSSA) were significantly lower and the NO levels were significantly higher among the stroke patients. XO showed a slight, nonsignificant increase in the patients, but the levels of MDA, NSSA, GRD, and GSH-Px did not show any significant differences between the two groups. The hemorrhage volume was negatively correlated with the initial score of the Glasgow Coma Scale and a positive correlation with lethal outcome, but it did not correlate significantly with any of the measured parameters. The results suggest that free radicals might play a role in the development of brain injury following brain hemorrhage.     

Nitric oxide levels and antioxidant enzyme activities in jaundices of premature infants

Free radicals are effective in the genesis of several diseases in the neonatal period. This study aimed to show the relationship between serum bilirubin levels and plasma nitric oxide and the activity of enzymes in the erythrocyte such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in premature infants. In the study, 20 premature infants with newborn jaundice were included and the control group was formed by 15 premature infants without jaundice. Venous blood samples were taken from all neonates in the study and control groups on the first day of hospitalization. Plasma nitric oxide levels and activities of SOD, GSH-Px and CAT enzymes in the erythrocytes were investigated in these samples. Plasma nitric oxide and serum bilirubin levels were found to be significantly higher in the study group (47.4 +/- 7.25 micromol l(-1), 18.41 +/- 3.28 mg dl(-1), respectively) than those in the control group (33.46 +/- 6.43 micromol l(-1), 4.35 +/- 0.60 mg dl(-1), respectively; p < 0.001). In addition, erythrocyte SOD, GSH-Px and CAT enzyme activities (724 +/- 78.61, 673 +/- 90.5, 63 +/- 12.8 U g(-1) Hb, respectively) were found to be significantly lower in the study group than those in the control group (1208 +/- 129.04, 1097.6 +/- 75.8, 99.06 +/- 12.4 U g(-1) Hb, respectively, p < 0.001). It was concluded that in the aetiology of hyperbilirubinemia, neonatal erythrocytes and nitric oxide reactions are affected differently and that erythrocyte haemolysis caused as a result of these effects may play a role in the aetiopathogenesis of unconjugated hyperbilirubinemia. Haemolysis may also be seen because of the inadequacy of the protection by erythrocytes against the cytotoxic effects of free radicals resulting from the lack of antioxidant enzymes in these cells.     

Lipid peroxidation and antioxidant enzyme levels in patients with schizophrenia and bipolar disorder

Recent data from several reports indicate that free radicals are involved in aetiopathogenesis of many human pathologies including neuropsychiatric disorders such as schizophrenia, bipolar disorder etc. In the present study, we aimed at determining and evaluating levels of malondialdehyde (MDA), a product of lipid peroxidation, and antioxidant enzyme superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity levels in patients diagnosed with schizophrenia (n = 25) and bipolar disorder (n = 23). The control group was composed of 20 healthy subjects. There was a significant increase in MDA levels of patients with schizophrenia and bipolar disorder compared with controls. SOD and GSH-Px activity levels were significantly higher in the schizophrenic group compared with controls. SOD activity levels in bipolar the group were significantly higher than controls whereas there were no significant changes in GSH-Px activity levels in the bipolar group and controls. Significant differences between lipid peroxidation product and antioxidant enzyme (SOD and GSH-Px) activity levels in schizophrenic and bipolar disorder patients compared with controls leads us to believe that these differences are related to the heterogenities in aetiologies of these disorders.     

Whole blood glutathione peroxidase and erythrocyte superoxide dismutase activities, serum trace elements (Se, Cu, Zn) and cardiovascular risk factors in subjects from the city of Ponta Delgada, Island of San Miguel, The Azores Archipelago, Portugal

Activities of whole blood glutathione peroxidase (GSH-Px) and erythrocyte superoxide dismutase (SOD) and serum levels of selenium (Se), copper (Cu) and zinc (Zn) were measured in 118 apparently healthy subjects aged 20-60 years from the city of Ponta Delgada, Island of San Miguel, The Azores Archipelago, Portugal. Data were analysed by age/gender, lipid profile and blood pressure as cardiovascular risk factors searching for their relevance when assessing reference values for antioxidant biomarkers. GSH-Px was in the same range, but SOD was significantly lower than in other Portuguese populations. Neither activity differed with gender. GSH-Px activity increased with age, namely in normolipidemic men versus the hyperlipidemic group in which a decrease was observed. This suggests a progressive impairment of GSH-Px with age caused by an enhanced production of oxidant species in hyperlipidemia. GSH-Px was 30% lower in male hypertensives versus normotensives. SOD activity did not relate to age or blood pressure but was 17% higher in the hyperlipidemic men versus the normolipidemic group, suggesting a better antioxidant protection by SOD than by GSH-Px in hyperlipidemia and hypertension. Se was higher in men versus women, particularly in the older subjects, and partly related to hyperlipidemia. Zn levels showed a similar dependency on gender, not related to age or lipid profile. Cu levels were much higher in women than in men in all age or lipid profile classes and decreased in hyperlipidemia. They were lowered with age in both genders, particularly in normolipidemic women. The present research therefore suggests that hyperlipidemia and hypertension do affect antioxidant status and should be considered when assessing antioxidant biomarkers in blood.