Erythrocyte Lipid Peroxidation Levels Research Articles

Glycosaminoglycan-induced proinflammatory cytokine levels as disease marker in mucopolysaccharidosis

Recently, it has been shown disturbances in oxidant/antioxidant system and increases in some inflammatory markers in animal studies and in some Mucopolysaccharidoses (MPSs) patients. In this study, we aimed to determine the oxidative stress/antioxidant parameters and pro-inflammatory cytokine levels in the serum of MPS patients, in order to evaluate the possible role of inflammation in these patient groups regarding to accumulated metabolites.MPS I (n = 3), MPS II (n = 8), MPS III (n = 4), MPS IVA (n = 3), MPS VI (n = 3), and VII (n = 1) patients and 20 age-matched healthy subjects were included into the study.There was no statistically significant change in activities of SOD, Catalase, GSH-Px and lipid peroxidation levels in erythrocytes between the MPS patients and healthy controls. While IL-1alpha (p = 0.054), IL-6 (p = 0.008) levels, and chitotriosidase activity (p = 0.003) elevated in MPS3 patients, IL1α (p = 0.006), IL-1β (p = 0.006), IL-6 (p = 0.006), IFNγ (p = 0.006), and NFκB (p = 0.006) levels increased in MPS-6 patients.Elevated levels of IL-6, IL1α and chitotriosidase activity demonstrated macrophage activation in MPSIII untreated with enzyme replacement. Our study showed for the first time that high levels of IL1α, IL-6, IL1β and NFκB were present in MPSVI patients, demonstrating the induction of inflammation by dermatan sulphate. The low level of paraoxonase in MPSVI patients may be a good marker for cardiac involvement.Overall, this study provides important insights into the relationship between lysosomal storage of glycosaminoglycan and inflammation in MPS patients. It highlights possible pathways for the increased release of inflammatory molecules and suggests new targets for the development of treatments.

Blood biochemistry and antioxidant status altered by anthropogenic impact in Adélie penguins (Pygoscelis adeliae).

Human activities are increased in Antarctica during decades, primarily due to the logistic and tourism operations, which consequent negative impact on penguin populations, altering their physiological responses. Therefore, we aimed to assess the blood biochemistry and oxidant/antioxidant balance of Adélie penguins (Pygoscelis adeliae) inhabiting two selected colonies: Potter Peninsula, considered as a low impacted colony, and Esperanza/Hope Bay as a high impacted colony. The levels of calcium, uric acid, and fructosamine, showed significant high values (p<0.05) for the Potter Peninsula´s penguins. Besides, this population showed high levels of plasma protein oxidation and erythrocyte lipid peroxidation (p<0.005) while the Esperanza/Hope Bay population presented high levels of erythrocyte protein oxidation and plasma lipid peroxidation (p<0.005). The oxidative damage values were similar in the Potter Peninsula population and slightly lower in the Esperanza/Hope Bay penguins if the results were compared to previous reports. The enzymes superoxide dismutase and glutathione peroxidase had significantly (p<0.005) high activity in the Esperanza/Hope Bay population, which also showed high reduced glutathione levels. The glutathione S-transferase activity was significantly high (p<0.005) in the Potter Peninsula population. The obtained results might take into account for making decisions about management and protection plans for the different penguin nesting areas in Antarctica.

Dietary supplementation with annatto food-coloring extracts increases the resistance of human erythrocytes to hemolysis

Erythrocytes exhibit high susceptibility to hemolysis in several pathologies due to the oxidation of cellular components. We hypothesized that annatto carotenoids improve the redox status of erythrocyte plasma membranes and promote a consequent increase in human erythrocyte resistance to hemolysis. The objective of this study was to evaluate whether food-grade annatto carotenoids can increase human erythrocyte resistance to hemolysis in vitro and ex vivo. For the in vitro experiment, erythrocytes from healthy volunteers were isolated and coincubated with bixin (BIX) or norbixin (NBIX) and 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH), glucose, or sodium nitrite (NaNO2) as hemolysis inducers. In the ex vivo study, healthy volunteers consumed a capsule containing BIX or NBIX (0.05 mg/kg body weight per day) or placebo for 7 days before blood sample collection. Their erythrocytes were isolated and incubated with AAPH, glucose, or NaNO2. In both the ex vivo and in vitro studies, erythrocytes were subjected to osmotic fragility tests. The activity of antioxidant enzymes, and reduced glutathione and lipid peroxidation levels in erythrocytes were also evaluated ex vivo. In vitro BIX and NBIX not only reduced erythrocyte membrane fragility induced by AAPH, glucose, or NaNO2 but also improved basal osmotic resistance in the micromole-per-liter range (P < .05). BIX and NBIX supplementation increased erythrocyte membrane resistance (P < .05), with BIX being more effective. Also, BIX and NBIX protected erythrocytes from lipid peroxidation and improved the cellular redox environment (P < .05). These results support the hypothesis that annatto carotenoids supplementation exerts antihemolytic properties by preventing the oxidative damage of human erythrocytes.

The catalase gene promoter and 5'-untranslated region variants lead to altered gene expression and enzyme activity in vitiligo.

Oxidative stress is considered to be the initial event in the course of vitiligo. The enzyme catalase (CAT) is mainly involved in cellular defence against oxidizing agents through detoxifying H2 O2 . The aims were (i) to assess erythrocyte CAT enzyme activity and lipid peroxidation (LPO) levels as well as CAT mRNA expression in skin and blood; (ii) to investigate CAT gene promoter rs7943316, rs1001179, 5'-untranslated region rs1049982, and exon (rs17886350, rs11032709, rs17880442, rs35677492) polymorphisms; and (iii) to perform genotype/haplotype-phenotype correlation analyses in patients with vitiligo and controls from Gujarat. CAT activity and LPO levels were measured spectrophotometrically. CAT mRNA levels were estimated using real-time polymerase chain reaction (PCR) by the SYBR Green method. Single-nucleotide polymorphism genotyping was performed using PCR-restriction fragment length polymorphism and amplification-refractory mutation system-PCR analyses. Patients with vitiligo showed significantly decreased CAT mRNA expression in lesional and nonlesional skin and in blood, with reduced CAT activity compared with that of controls. CAT -89A/T and -20T/C polymorphisms were significantly associated with patients, especially with active and generalized vitiligo, whereas no association was observed for -262G/A and exon polymorphisms. The A-262 T-89 C-20 haplotype with variant alleles was found to be associated with 6·4-fold risk of vitiligo. Genotype/haplotype-phenotype correlation analyses revealed that individuals with susceptible genotypes/haplotype for CAT -89A/T and -20T/C polymorphisms showed significantly decreased CAT mRNA/activity, and only -89A/T polymorphisms showed significantly increased LPO levels compared with wild-type genotypes/haplotype. The present study proposes the crucial role of CAT and its allelic variants in oxidative stress-mediated pathogenesis of vitiligo.

Different doses of dexmedetomidine reduce plasma cytokine production, brain oxidative injury, PARP and caspase expression levels but increase liver oxidative toxicity in cerebral ischemia-induced rats.

Cerebral ischemia-induced progression of brain, liver, and erythrocyte oxidative injuries might be modulated by dexmedetomidine (DEX) as a potent antioxidant and anti-inflammatory drug. The present study was conducted to explore whether two different doses of DEX protect against plasma cytokine and brain, liver and erythrocyte oxidative toxicity and apoptosis in cerebral ischemia-induced rats. Forty-two rats were equally divided into 7 groups. The first and second groups were used as untreated and sham controls, respectively. The third (DEX4) and fourth (DEX40) groups received 4mg/kg and 40mg/kg DEX treatments. The fifth, sixth and seventh group were operated on to induce cerebral ischemia. The fifth, sixth and seventh groups are used to represent cerebral ischemia, cerebral ischemia+DEX4, and cerebral ischemia+DEX40, respectively. DEX was intraperitoneally given to the DEX groups at the 3rd, 24th and 48th hour. Brain and erythrocyte lipid peroxidation (MDA) levels and plasma IL-1β and TNF-α levels were high in the cerebral ischemia group although they were low in the DEX4 and DEX40 groups. Decreased glutathione peroxidase (GSH-Px) and reduced glutathione (GSH) values in the brain and erythrocyte of the cerebral ischemia group were increased by the DEX treatments, although PARP, and the caspase 3 and 9 expressions in the brain were further decreased. Conversely, the cerebral ischemia-induced decrease in the liver vitamin A, vitamin E, GSH, and GSH-Px were further decreased by the DEX treatments, although MDA level, PARP, and caspase 3 and 9 expressions were further increased by the DEX treatments. In conclusion, DEX induced protective effects against cerebral ischemia-induced brain and erythrocyte oxidative injuries through regulation of the antioxidant level and cytokine production. However, both doses of DEX induced oxidative toxicity and apoptotic effects in the rats' livers.

Selenium attenuates apoptosis, inflammation and oxidative stress in the blood and brain of aged rats with scopolamine-induced dementia.

A potent antioxidant, selenium might modulate dementia-induced progression of brain and blood oxidative and apoptotic injuries. The present study explores whether selenium protects against experimental dementia (scopolamine, SCOP)-induced brain, and blood oxidative stress, apoptosis levels, and cytokine production in rats. Thirty-two rats were equally divided into four groups. The first group was used as an untreated control. The second group was treated with SCOP to induce dementia. The third and fourth groups received 1.5mg/kg selenium (sodium selenite) and SCOP+selenium, respectively. Dementia was induced in the second and forth groups by intraperitoneal SCOP (1mg/kg) administration. Brain, plasma, and erythrocyte lipid peroxidation levels as well as plasma TNF-α, interleukin (IL)-1β, and IL-4 levels were high in the SCOP group though they were low in selenium treatments. Selenium and selenium+SCOP treatments increased the lowered glutathione peroxidase activity, reduced glutathione, vitamins A and E concentrations in the brain, erythrocytes and plasma of the SCOP group. Apoptotic value expressions as active caspase-3, procaspase-9, and PARP were also increased by SCOP, while they were decreased by selenium and selenium+SCOP treatments. In conclusion, selenium induced protective effects against experimental dementia-induced brain, and blood oxidative injuries and apoptosis through regulation of cytokine production, vitamin E, glutathione concentrations, and glutathione peroxidase activity.

Raloxifene and Tamoxifen Reduce PARP Activity, Cytokine and Oxidative Stress Levels in the Brain and Blood of Ovariectomized Rats.

It is well known that 17β-estradiol (E2) has an antioxidant role on neurological systems in the brain. Raloxifene (RLX) and tamoxifen (TMX) are selective estrogen receptor modulators. An E2 deficiency stimulates mitochondrial functions for promoting apoptosis and increasing reactive oxygen species (ROS) production. However, RLX and TMX may reduce the mitochondrial ROS production via their antioxidant properties in the brain and erythrocytes of ovariectomized (OVX) rats. We aimed to investigate the effects of E2, RLX, and TMX on oxidative stress, apoptosis, and cytokine production in the brain and erythrocytes of OVX rats.Forty female rats were divided into five groups. The first group was used as a control group. The second group was the OVX group. The third, fourth, and fifth groups were OVX + E2, OVX + TMX, and OVX + RLX groups, respectively. E2, TMX, and RLX were given subcutaneously to the OVX + E2 and OVX + TMX, OVX + RLX groups for 14days after the ovariectomyrespectively.While brain and erythrocyte lipid peroxidation levels were high in the OVX group, they were low in the OVX + E2, OVX + RLX, and OVX + TMX groups. OVX + E2, OVX + RLX, and OVX + TMX treatments increased the lowered glutathione peroxidase activity in erythrocytes and the brain and reduced glutathione and vitamin E concentrations in the brain. β-carotene and vitamin A concentrations in the brain and TNF-α and interleukin (IL)-1β levels in the plasma of the five groups were not significantly changed by the treatments. However, increased plasma IL-4 levels and Western blot results for brain poly (ADP-ribose) polymerase (PARP) in the OVX groups were decreased by E2, TMX, and RLX treatments, although proapoptotic procaspase 3 and 9 activities were increased by the treatments.In conclusion, we observed that E2, RLX, and TMX administrations were beneficial on oxidative stress, inflammation, and PARP levels in the serum and brain of OVX rats by modulating antioxidant systems, DNA damage, and cytokine production.

Melatonin and selenium reduce plasma cytokine and brain oxidative stress levels in diabetic rats

Background: Hyperglycaemia-induced progression of brain and erythrocyte oxidative injuries might be modulated by melatonin and selenium as potent antioxidants. The present study was conducted to explore whether melatonin and selenium protect against diabetic brain and erythrocyte oxidative stress levels in streptozotocin (STZ)-induced diabetic rats.Materials and methods: Seventy rats were equally divided into seven groups. The first and second groups were used as untreated and placebo treated controls. The third group was treated with STZ to induce diabetes. The fourth and sixth groups received 10 mg kg−1 melatonin. The fifth and seventh groups were treated with 1.5 mg kg−1 selenium (sodium selenite). The sixth and seventh groups were treated with STZ administered with melatonin and selenium as described for the fourth and fifth groups.Results: Brain and erythrocyte lipid peroxidation levels and plasma IL-1β and IL-4 levels were high in the STZ group, although they were low in melatonin and selenium treatments. Decreased glutathione peroxidase, reduced glutathione, total antioxidant status, vitamins A and vitamin E values in brain and erythrocyte of STZ group were increased by melatonin and selenium treatments.Discussion: Melatonin and selenium induced protective effects against diabetes-induced brain and erythrocyte oxidative injuries through regulation of the antioxidant level and cytokine production.

Chlorpyrifos induced toxicity in reproductive organs of female Wistar rats

Chlorpyrifos (CPF) is an organophosphate (OP) insecticide extensively used in agricultural and domestic settings. Healthy adult female albino rats were divided into three groups of six rats in each. Two groups were dosed orally with CPF in vegetable oil (0.1 and 2.5mg/kg/day) and third group was given vegetable oil for 8weeks. Non-significant changes were observed for body weight and feed intake. A disruption in estrous cyclicity was observed with a prolonged metestrous. Erythrocyte osmotic fragility and lipid peroxidation levels increased significantly. Mammary gland whole mounts revealed a significant (P<0.05–0.0001) increase in the ductal thickness, number of branches, alveolar and terminal end bud number and terminal end bud diameter. A significant increase in ovarian surface epithelium height, follicular diameter and follicular atresia was observed in treated rats (P<0.05–0.0001). A similar significant increase in the uterine surface epithelium height, endometrial gland epithelium height and myometrium thickness in higher dose group was recorded (P<0.05–0.0001). Luminal epithelium height and endometrial gland diameter was increased significantly in both the treated groups (P<0.05–0.0001). The results indicate that sub-chronic exposure of CPF causes oxidative stress and negative effects on the reproductive organs of female rats, which may be a pointer towards beginning of cancer incidence.

Selenium and Topiramate Attenuates Blood Oxidative Toxicity in Patients with Epilepsy: A Clinical Pilot Study

It is well known that oxidative stress plays an important role in the etiology of epilepsy. We investigated effects of selenium (Se) and topiramate (TPM) combination supplementation on antioxidant and oxidant values in control and patients with epilepsy and refractory epilepsy. For the aim, we used control (n = 19), epilepsy + TPM (n = 19), epilepsy + TPM + Se (n = 15) groups. We also used control (n = 15), refractory epilepsy (n = 15), and refractory epilepsy + Se (n = 8) groups. TPM (0.2 mg/daily) and Se, as sodium selenite (twice daily with 0.1 mg doses), were orally supplemented to the patients for 45 days. Erythrocyte lipid peroxidation levels were higher in refractory epilepsy groups than in control although its level and seizure numbers were decreased in TPM and TPM + Se supplemented groups of the patients. The erythrocyte reduced glutathione (GSH), glutathione peroxidase (GSH-Px), plasma total antioxidant status (TAS), and vitamin E concentration in refractory epilepsy group were lower than in control. However, the erythrocyte and plasma TAS, erythrocyte GSH and GSH-Px, and plasma vitamins A and C values were increased either by Se or Se + TPM in epilepsy and refractory epilepsy groups. There were no effects of TPM and Se on plasma β-carotene values in the groups. In conclusion, TPM and selenium caused protective effects on the epilepsy and refractory epilepsy-induced oxidative injury by inhibiting free radical production and supporting antioxidant redox system.

Oxidative Stress and Antioxidant Status in Acute and Chronic Myeloid Leukemia Patients

Oxidative stress, a pervasive condition of increased number of reactive oxygen species, is now recognized to be prominent feature of various diseases and their progression. The relationship between antioxidants and levels of well-known markers of oxidative stress, measured as lipid peroxides and oxidized proteins reflect health indices. The aim of this study is to evaluate the extent of oxidative stress and antioxidant status in acute and chronic myeloid leukemia patients. The present study included 60 patients selected using standard questionnaire based on age, family history, Body Mass Index (BMI), dietary intake, with no other complications and 30 age and sex-matched healthy subjects. The median age of myeloid leukemia patients was 43 years and that of controls was 42 years. Out of 60 myeloid leukemia patients, 30 were in acute and 30 were in chronic state. Oxidative stress and antioxidant status were evaluated in the patients and in the controls by assessing standard oxidative stress markers viz. plasma and erythrocyte lipid peroxide levels in terms of malondialdehyde and oxidized proteins as protein carbonyls whereas antioxidant status was assessed in terms of serum non enzymatic antioxidant levels. There was a significant increase (p 0.01) in plasma and erythrocyte lipid peroxidation and protein oxidation in acute and chronic myeloid leukemia patients as compared to healthy subjects. Antioxidant status as indicated by the levels of non-enzymatic antioxidants viz. erythrocyte reduced glutathione (GSH), serum β carotene, vitamin A & C and ceruloplasmin was found to be significantly decreased (p 0.01) in both the leukemia patients as compared to healthy participants. However, chronic myeloid leukemia patients had significantly (p 0.05) higher oxidative stress and lower antioxidant status as compared to acute myeloid leukemia patients.

Effect of luteolin on lipid peroxidation and antioxidants in acute and chronic periods of isoproterenol induced myocardial infarction in rats

The present study was designed to investigate the preventive effect of luteolin on lipid peroxidation, antioxidants and histopathological findings in acute and chronic periods after isoproterenol (ISO)-induced myocardial-infarction (MI) in male Wistar rats. Luteolin supplemented by intragastric intubation at a daily dose of 0.3 mg/kg body weight in acute and chronic periods following MI. In acute MI model, luteolin had been administered once per day to rat groups during 30 days. On days 29 and 30th the rats of the acute MI control groups were administered 85mg/kg body weight, isoproterenol, intraperitoneally intravel of 24h. In chronic MI model luteolin administered of rat group during 30 days, and on the 1st and 2nd days, the rats of the chronic MI control and luteolin treatment groups were administered ISO by the same way. The ISO-induced rats both in acute and chronic models showed significant increase in the levels of thiobarbituric acid reactive substances, lipid hydroperoxides in the heart and erythrocyte, and significant decrease in the activities of heart and erythrocytes superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione. Oral treatment with luteolin at a daily dose of (0.3 mg/kg b.wt) in both acute and chronic models showed significant decrease in the levels of heart and erythrocyte lipid peroxidation by products and significant increase in the levels of antioxidant system. The protective role of luteolin (0.3 mg/kg b.wt) on ISO-induced myocardial infarction was further confirmed by histopathological examination. Thus, the experiment clearly showed that luteolin ameliorates cardiac damage in ISO-induced myocardial infarction by prevented the accumulation of lipids due to the anti-lipid peroxidative effect.

EFFECT OF ZOBO DRINK (HIBISCUS SABDARIFFA WATER EXTRACT) ON BIOCHEMICAL AND HEMATOLOGICAL PARAMETERS IN MALE CYCLISTS

The aim of the present study was to evaluate, in a group of male cyclists the effects of short-term consumption of aqueous extract of the dried calyx of Hibiscus sabdariffa (popularly referred to as zobo in Nigeria) on some hematological and biochemical indices. Mmale clyclists who consumed the placebo (test control group) had significantly reduced hemoglobin (Hb) concentration, packed cell volume (PCV) and red blood cell (RBC) count, while the white blood cell (WBC) was signifi- cantly increased relative to inactive control subjects after one and two months of study. These pa- rameters were restored to a level comparable to controls in the group of cylists who consumed zobo drink (test group) for one and two months. The levels of erythrocyte superoxide dismutase (SOD), catalase (CAT) and lipid peroxidation (LPO) were significantly elevated in cyclists in the test control group relative sedentary controls after both durations of the study. These parameters were restored toward control values after two months of ingestion of zobo drink. The lactate dehy- drogenase activity in the erythrocyte of the cyclist was significantly high with or without zobo in- gestion relative to control after both durations of the study. In conclusion, the results obtained indi- cate that consumption of zobo drink (which is rich in antioxidants and other components) may be beneficial to athletes as it restored the exercise induced alterations of some hematological and bio- chemical parameters in cyclists under regular training.

Membrane Lipid Peroxidation of HbAA Erythrocyte of Non-Malarious Participants Administered with Quinine

The erythrocyte membrane is susceptible to lipid peroxidation due to its high content of polyunsaturated lipids. The present study ascertained levels of lipid peroxidation of non-parasitized erythrocytes of non-malarious male participants administered with quinine. Determination of erythrocyte lipid peroxidation was by a monitor of levels of thiobarbituric acid reactive substances, measured spectrophotometrically by taking the sample absorbance at 432 nm against a reagent blank at 24 °C. Fifteen (15) non-malarious male (59–79 kg) participants of confirmed HbAA genotype between the age brackets of 21–34 yr enrolled for this study. Three (3) participants per group were administered with quinine according to the corresponding doses: 1.5, 3.0, 4.5 and 6.0 mg/kg (control; n = 3). At regular time interval of 3 h for 12 h, blood samples were withdrawn for determination of erythrocyte membrane lipid peroxidation. Erythrocyte membrane of participants administered with quinine exhibited relatively high levels of lipid peroxidation in a dose dependent manner. Generally, within 0–6 h, the four adminstered doses of quinine caused a time dependent elevation of lipid peroxidation. Further increase in time (t > 6 h) showed decreasing levels of lipid peroxidation in participants administered with quinine. Generally, the levels of erythrocyte lipid peroxidation in the presence of quinine showed 2 phase profile. The first stage showed increasing levels of lipid peroxidation at t < 6 h after drug administration, followed by the second phase which showed decreasing levels of lipid peroxidation. The results showed that administration of quinine to non-malarious individuals elicited flux in erythrocyte lipid peroxidation.

Effects of swimming on erythrocyte rheological properties

Exercise and lactate usually change blood rheology but, effect of swimming on blood rheology is not clear. Blood lactate concentration increases after 400-meter freestyle swimming. In the hemorheological studies, determination of the erythrocyte deformability and aggregation facilitates the evaluation of rheological behaviours of the erythrocytes. The present study was performed to investigate the effects of acute swimming exercise on erythrocyte deformability and aggregation. Seventeen male university swimmers participated in the study. For 400-meter freestyle swimming, participants were asked to swim as fast as they could. Blood lactate concentration, erythrocyte lipid peroxidation and plasma protein oxidation levels, erythrocyte deformability and aggregation, and several haematological parameters were investigated after swimming and they were compared with pre-exercise values. Erythrocyte lipid peroxidation and plasma protein oxidation were unchanged with swimming. Blood lactate concentration increased after 400-meter swimming (p<0.001). Erythrocyte aggregation increased after acute swimming (p<0.01) while erythrocyte deformability was not change. There were no correlations between blood lactate and erythrocyte hemorheological properties before and after swimming. In conclusion, we found that erythrocyte aggregation increased after acute swimming. Further studies are needed to reveal the late effects of acute swimming and to elucidate the effect of swimming different distances on erythrocyte rheological properties.

Effects of Vitamin C and E Combination on Element and Oxidative Stress Levels in the Blood of Operative Patients Under Desflurane Anesthesia

We investigated effects of vitamin C and E (VCE) administration on desflurane-induced oxidative toxicity and element changes in the blood of operative patients under desflurane general anesthesia. Forty American Society of Anesthesiologists I or II Physical Status adult patients were scheduled for elective surgery. The patients were randomly divided into two groups. Control and VCE group was introduced to anesthesia with desflurane. VCE was administreted to patients in the control and VCE group before 1 hour of anesthesia with desflurane. Baseline (preoperative) and postoperative (at the 1(st), the 24(th), and 72(th) h), blood samples were taken from the first and second groups. Erythrocyte and plasma lipid peroxidation levels at the 1(st), 24(th), and 72(th) hours were higher in the control than in baseline group, although their levels at the same periods were lower in the VCE group than in the control. Vitamin E levels at the postoperative 1(st) and 24(th) hours and erythrocyte glutathione peroxidase (GSH-Px) activity at the postoperative 1(st), 24(th), and 72(th) hours was lower than in baseline values. Erythrocyte GSH-Px activity and plasma vitamins A, C, and E levels at the postoperative 1(st), 24(th), and 72(th) hours were higher in the VCE group than in the control group. Erythrocyte and plasma reduced glutathione, plasma β-carotene, and serum copper, while zinc, selenium, aluminum, iron, magnesium, and calcium levels did not differ between preoperative and postoperative periods in both groups. In conclusion, VCE combination prevented the desflurane-induced vitamin E and GSH-Px consumptions to strengthen the antioxidant levels in the blood of operative patients.

Antioxidant effect of ethanol extract of powdered grape skin in C57BL/6J mice fed high‐fat diet

Grape seeds and skins are good sources of phytochemicals such as gallic acid, catechin, and epicatechin and are suitable raw materials for the production of antioxidative dietary supplements. And grape skins were a much more potent source than either grape pulp, juice or seeds. This study investigated the effect of ethanol extract of powdered grape skin antioxidant metabolism in high fat fed C57BL/6J mice. Five‐week‐old male C57BL/6J mice were randomly divided into two groups and fed high‐fat diet (HF control, 20%fat(w/w)) and with ethanol extract of powdered grape skin(GS) for 9 weeks. The plasma total cholesterol concentration was significantly higher in the HF group. Hepatic glutathione reductase, erythrocyte superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase activities were significantly higher in the GS group than in the HF group. Erythrocyte thiobarbituric reactive substances (TBARS) level was tended to be lower in the GS group than in the HF group. Therefore, we suggest that grape skin is effective material on improvement of antioxidant metabolsim because GS supplementation induced the elevation of hepatic antioxidant enzyme activities, the reduction of erythrocyte lipid peroxide levels and hypocholesterolemic effects in high‐fat‐fed mice.

Melatonin Modulates Hippocampus NMDA Receptors, Blood and Brain Oxidative Stress Levels in Ovariectomized Rats

We investigated the effects of melatonin administration on ovariectomy-induced oxidative toxicity and N-methyl-D: -aspartate receptor (NMDAR) subunits in the blood of rats. Thirty-two rats were studied in three groups. The first and second groups were control and ovariectomized rats. Melatonin was daily administrated to the ovariectomized rats in the third group for 30 days. Blood, brain cortical and hippocampal samples were taken from the three groups after 30 days. Brain cortical, erythrocyte and plasma lipid peroxidation (LP) levels were higher in the ovariectomized group than in controls, although the LP level was decreased in the ovariectomized group with melatonin treatment. Brain cortical and plasma concentrations of vitamins A, C and E as well as the NMDAR 2B subunit were lower in the ovariectomized group than in controls, although, except for plasma vitamin C, they were increased by the treatment. Brain cortical and erythrocyte reduced glutathione (GSH) levels were lower in the ovariectomized group than in controls, although erythrocyte GSH levels were higher in the melatonin group than in the ovariectomized group. Brain cortical and erythrocyte glutathione peroxidase activity and NMDAR 2A subunit concentrations were not found to be different in all groups statistically. Oxidative stress has been proposed to explain the biological side effect of experimental menopause. Melatonin prevents experimental menopause-induced oxidative stress to strengthen antioxidant vitamin and NMDAR 2A subunit concentrations in ovariectomized rats.

P121 Erythrocyte lipid peroxidation and antioxidant enzyme levels in patients with febrile convulsion

P121 Erythrocyte lipid peroxidation and antioxidant enzyme levels in patients with febrile convulsion

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.