Increased Plasma Lipid Peroxidation Research Articles

Carotid body and cardiorespiratory alterations in intermittent hypoxia: the oxidative link

Intermittent hypoxia, a feature of obstructive sleep apnoea, potentiates ventilatory hypoxic responses, alters heart rate variability and produces hypertension, partially owing to an enhanced carotid body responsiveness to hypoxia. Since oxidative stress is a potential mediator of both chemosensory and cardiorespiratory alterations, we hypothesised that an antioxidant treatment may prevent these alterations. Accordingly, we studied the effects of ascorbic acid (1.25 g.L(-1) drinking water) on plasma lipid peroxidation, nitrotyrosine and inducible nitric oxide synthase (iNOS) immunoreactivity in the carotid body, ventilatory and carotid chemosensory responses to acute hypoxia, heart rate variability and arterial blood pressure in male Sprague-Dawley rats exposed to 5% O(2); 12 episodes.h(-1); 8 h.day(-1) or sham condition for 21 days. Intermittent hypoxia increased plasma lipid peroxidation, nitrotyrosine and iNOS expression in the carotid body, enhanced carotid chemosensory and ventilatory hypoxic responses, modified heart rate variability and produced hypertension. Ascorbic acid prevented the increased plasma lipid peroxidation and nitrotyrosine formation within the carotid body, and the enhanced carotid chemosensory and ventilatory responses to hypoxia, as well as heart rate variability alterations and hypertension. The present results support an essential role for oxidative stress in the generation of carotid body chemosensory potentiation and systemic cardiorespiratory alterations induced by intermittent hypoxia.

Investigation of Lipid Profiles and Lipid Peroxidation in Patients with Type 2 Diabetes

The aim of this study was to investigat the lipid peroxidation of plasma as a marker of oxidant-induced protein damage the effects of oxygen radicals on glycated-hemoglobin and to find out the relationship between the increase level of Malondialdehyde (MDA) on HbA1C, lipid profiles and FBS (Fasting Blood Sugar) in patients with type 2 diabetes. This randomized study included 200 individuals, 100 cases had history of diabetic for at least 3 years (file in Isfehan hospital, Diabetic Center of Medical Sciences University) and 100 cases as the control group without history of diabetes. In both groups, level of MDA, FBS, lipid profiles and HbA1C were determined in fasting blood samples. Results showed that MDA level in diabetic patients was significantly (p<0.005) higher (0.9222 ± 0.3 μmol/L) than those in the control group (0.7428 ± 0.04μmol/L). The same was also true (p<0.05) for the level of HbA1C (9.387 ± 2.4 mg/dl in diabetic patients and 7.356 ± 1.0 mg/dl in the control group) and the FBS (163.31 ± 56mg/dl in patient group and 85.740 ± 10.1 in the control group). Furthermore, the concentration of, LDL significantly was higher (p<0.05) and the HDL level were significantly lower (p<0.05) in case group as compared to control group. The increased plasma lipid peroxidation and decreased plasma HDL that we observed in patients with type 2 diabetes mellitus indicated that these may predispose to the development of cardiovascular complications. © EuroJournals Publishing, Inc. 2009.

Enhanced Butyrylcholinesterase Activity may be the Common Link in Triggering Low-Grade Systemic Inflammation and Decrease in Cognitive Function in Diabetes Mellitus and Alzheimers disease

There is increasing evidence that diabetes mellitus and Alzheimer's disease occur more often than by chance. Recently, we proposed that increase in the activity of the enzyme butyrylcholinesterase could be a common link between these two conditions. Acetylcholine is an anti-inflammatory molecule. Butyrylcholinesterase by inactivating acetylcholine may enhance inflammation and induce decline in cognitive function. In the present study, it was noted that streptozotocin- induced diabetic animals showed dyslipidemia, increase in plasma lipid peroxides, decrease in circulating plasma superoxide dismutase activity, decline in cognitive function as assessed by the Morris water maze method, and a significant increase in serum butyrylcholinesterase activity. These results suggest that increased plasma and, possibly, tissue concentrations of butyrylcholinesterase lead to decrease in acetylcholine levels, an anti-inflammatory molecule, which may trigger low-grade systemic inflammation in diabetes mellitus and Alzheimer's disease that could account for decline in cognitive function.

Oxidative damage of rat liver induced by ligature-induced periodontitis and chronic ethanol consumption

Objective Oxidative stress plays a central role in the initiation and progression of liver disease. Chronic ethanol consumption induces oxidative damage of the liver. Using a rat model, we previously showed that chronic administration of lipopolysaccharide and proteases to gingival sulcus induced both periodontal inflammation and liver injury. Periodontitis and ethanol consumption may have an additional effect on hepatic oxidative damage. The present study investigated the effects of periodontitis on ethanol-induced oxidative damage of the liver using a rat model. Design Male Wistar rats were divided into four groups (six rats/group). During the experimental period of eight weeks, two groups were fed an ethanol-containing liquid diet, and two groups were on a pair-fed control diet. Four weeks prior to the end of the experimental period, one group from each dietary treatment was ligated to induce periodontitis, while the other group was left unligated. In order to evaluate hepatic oxidative damage, the level of hexanoyl-lysine and the ratio of reduced form glutathione/oxidized form glutathione (GSH/GSSG) was determined. The concentration of blood hexanoyl-lysine was also measured as an index of circulating lipid peroxide. Results Ligature-induced periodontitis increased plasma levels of hexanoyl-lysine. In the liver, periodontitis decreased the GSH/GSSG ratio, and the combination of periodontitis and ethanol consumption induced a significant increase in hexanoyl-lysine level compared to ethanol consumption alone. Conclusion In the rat model, ligature-induced periodontitis increased plasma lipid peroxide, decreased the hepatic GSH/GSSG ratio and augmented ethanol-induced lipid peroxidation in the liver.

Analysis of the effects of exposure to acute hypoxia on oxidative lesions and tumour progression in a transgenic mouse breast cancer model

BackgroundTumour hypoxia is known to be a poor prognostic indicator, predictive of increased risk of metastatic disease and reduced survival. Genomic instability has been proposed as one of the potential mechanisms for hypoxic tumour progression. Both of these features are commonly found in many cancer types, but their relationship and association with tumour progression has not been examined in the same model.MethodsTo address this issue, we determined the effects of 6 week in vivo acute hypoxic exposure on the levels of mutagenic lipid peroxidation product, malondialdehyde, and 8-oxo-7,8-dihydro-2'-deoxyguanosine DNA (8-oxo-dG) lesions in the transgenic polyomavirus middle T (PyMT) breast cancer mouse model.ResultsWe observed significantly increased plasma lipid peroxidation and 8-oxo-dG lesion levels in the hypoxia-exposed mice. Consumption of malondialdehyde also induced a significant increase in the PyMT tumour DNA lesion levels, however, these increases did not translate into enhanced tumour progression. We further showed that the in vivo exposure to acute hypoxia induced accumulation of F4/80 positive tumour-associated macrophages (TAMs), demonstrating a relationship between hypoxia and macrophages in an experimental model.ConclusionThese data suggest that although exposure to acute hypoxia causes an increase in 8-oxo-dG lesions and TAMs in the PyMT tumours, these increases do not translate into significant changes in tumour progression at the primary or metastatic levels in this strong viral oncogene-driven breast cancer model.

Role of superoxide and hydrogen peroxide in hypertension induced by an antagonist of adenosine receptors

Treatment of Wistar rats for 7 days with 1,3-dipropyl-8-sulfophenylxanthine (DPSPX), an antagonist of adenosine receptors, induces long-lasting hypertension associated with marked changes in vascular structure and reactivity and renin–angiotensin system activation. This study aimed at evaluating the role of oxidative stress in the development of DPSPX-induced hypertension and also at identifying the relative contribution of superoxide radical (O 2 •−) vs hydrogen peroxide (H 2O 2). Vascular and systemic prooxidant/antioxidant status was evaluated in sham (saline, i.p., 7 days) and DPSPX (90 μg/kg/h, i.p., 7 days)-treated rats. Systolic blood pressure was determined by invasive and non-invasive methods. The activity of vascular NADPH oxidase, superoxide dismutase (SOD), catalase and glutathione peroxidase was assayed by fluorometric/spectrophotometric methods. H 2O 2 levels were measured using an Amplex Red Hydrogen Peroxide kit. Plasma thiobarbituric acid reactive substances and plasma antioxidant capacity were also measured. In addition we tested the effects of antioxidants or inhibitors of reactive oxygen species generation on blood pressure, vascular hyperplasia and oxidative stress parameters. DPSPX-hypertensive rats showed increased activity of vascular NADPH oxidase, SOD, catalase and glutathione peroxidase, as well as increased H 2O 2 generation. DPSPX-hypertensive rats also had increased plasma lipid peroxidation and decreased plasma antioxidant capacity. Treatment with apocynin (1.5 mmol/l, per os, 14 days), or with polyethylene glycol (PEG)-catalase (10,000 U/kg/day, i.p., 8 days), prevented the DPSPX-induced effects on blood pressure, vascular structure and H 2O 2 levels. Tempol (3 mmol/l, per os, 14 days) failed to inhibit these changes, unless PEG-catalase was co-administered. It is concluded that O 2 •− generation with subsequent formation of H 2O 2 plays a major role in the development of DPSPX-induced hypertension.

Effect of chromium(VI) on the status of plasma lipid peroxidation and erythrocyte antioxidant enzymes in chromium plating workers

The present study was carried out to determine the effect of chromium(VI) on the status of plasma lipid peroxidation and erythrocyte antioxidant enzymes in workers exposed to chromium during chromium plating process. Fifty subjects working in chromium plating process formed the study group. An equal number of age-sex matched subjects working in administrative units formed the control group. The control subjects were residing in the same city but away from the work place of study group subjects. Urinary chromium levels were determined by using a graphite furnace atomic absorption spectrophotometer. The plasma lipid peroxidation and erythrocyte antioxidant enzymes were determined by using spectrophotmetric methods. A significant increase of plasma lipid peroxidation and a significant decrease of superoxide dismutase and glutathione peroxidase levels were noted in the study group as compared with the controls. The level of plasma lipid peroxidation was positively and erythrocyte antioxidant enzymes were negatively and significantly correlated with chromium levels in urine. Multiple regression analysis was assessed the oxidative stress associated with chromium and life style confounding factors such as BMI, coffee, tea, alcohol and smoking. The multiple regression analysis showed that the urine chromium levels >10 micro g/g of creatinine, smoking, consumption of green vegetables and BMI variables were significantly associated with the levels of oxidative stress. The results show that the increased plasma lipid peroxidation and decreased antioxidant enzymes (superoxide dismutase and glutathione peroxidase) observed in chromium-exposed workers could be used as biomarkers of oxidative stress.

Plasma lipid peroxidation and erythrocyte antioxidant enzymes status in workers exposed to cadmium

Cadmium (Cd) is a corrosion-resistant metal, used extensively for electroplating in the automobile, electronic and aerospace industry. Only a few studies are available regarding Cd-induced oxidative stress in animals, but no reports are available regarding the effects of Cd on oxidative stress during occupational exposure. The present study was carried out to determine the plasma lipid peroxidation and erythrocyte antioxidant enzymes status in workers exposed to Cd during electroplating. 50 subjects exposed to Cd during electroplating formed the study group. An equal number of age-sex matched subjects, working in the administrative section, formed the control group. Urinary Cd levels were determined using the flameless atomic absorption spectrophotometer. Plasma lipid peroxidation and erythrocyte antioxidant enzymes were determined using spectrophotometric methods. A significant increase of plasma lipid peroxidation and a significant decrease of superoxide dismutase and glutathione peroxidase levels were noted in the study group compared with the control group. The level of plasma lipid peroxidation was positively and erythrocyte antioxidant enzymes were negatively and significantly associated with Cd levels in urine. Multiple regression analysis assessed the oxidative stress associated with Cd and other lifestyle confounding factors, such as age, body mass index, the consumption of vegetables, coffee, tea, smoking and alcohol. Analysis showed that the lifestyle confounding factors viz; smoking, body mass index and urinary Cd levels > 5 microg/g of creatinine, were significantly associated with oxidative stress. The results of the present study suggest that increased plasma lipid peroxidation and decreased superoxide dismutase levels could be used as biomarkers of oxidative stress in cadmium-exposed workers.

Influence of Vitamin C and E Supplementation on Oxidative Stress Induced by Hyperbaric Oxygen in Healthy Men

Aim: To investigate the effect of a 4-week vitamin C and E supplementation on oxidative stress induced by hyperbaric oxygen (HBO). Methods: 19 healthy men were exposed to 3 sequential protocols, i.e. HBO (100% O₂, 2.4 bar, 131 min) before (T1) and after 4 weeks of daily supplementation with 500 mg slow-release vitamin C and 272 IU vitamin E (T2). A normoatmospheric protocol (21% O₂, 1.0 bar, 131 min) served as control treatment (nonexposed). Blood samples were taken before (B) and immediately after (A) treatment. Plasma levels of vitamin A, C, E, β-carotene, reduced glutathione and malondialdehyde were measured by HPLC. Antioxidative capacity and lipid peroxides in plasma were analyzed by ELISA. Results: HBO decreased vitamin C and antioxidative capacity (T1). At T1, Δ A – B of vitamin C and lipid peroxides was different from nonexposed. Vitamin supplementation increased plasma levels of vitamin C and E by 28 and 37%, respectively. Vitamin supplementation led to decreased concentrations of lipid peroxides and reduced glutathione. After supplementation, HBO decreased vitamin C and reduced glutathione. At T2, Δ A – B of vitamin C and lipid peroxides was significantly different from nonexposed. Conclusion: In humans, oxidative stress decreased plasma levels of vitamin C and antioxidative capacity and increased plasma lipid peroxides. Supplementation with vitamin C and E did not prevent these effects.

Plasma lipid peroxidation and erythrocyte antioxidants status in workers exposed to nickel

The objectives were to investigate the plasma lipid peroxidation and erythrocyte antioxidants status in workers exposed to nickel. The study groups comprised 69 nickel plating workers and 50 office workers residing in the same city, but away from the place of work of the study group subjects, considered as control group. Urinary nickel concentration was determined by graphite furnace atomic absorption spectrophotometry. The plasma lipid peroxidation and erythrocyte antioxidants were measured by spectrophotmetric methods. The plasma lipid peroxidation level was significantly increased in nickel-platers and their helpers as compared with controls. Erythrocyte antioxidants were significantly decreased in the nickel-platers compared with the controls. The level of plasma lipid peroxidation was positively and erythrocyte antioxidants were negatively and significantly correlated with the urine nickel levels. Multiple regression analysis assessed the oxidative stress associated with nickel and other potential confounding factors such as body mass index, the consumption of green vegetables, coffee, tea, smoking and alcohol consumption. Analysis showed that the lifestyle confounding factors: the consumption of green vegetables, smoking and alcohol, were not significantly associated with oxidative stress. The exposure to nickel, body mass index and coffee consumption were significantly associated with oxidative stress. The results show that the increased plasma lipid peroxidation and decreased erythrocyte antioxidants levels observed in nickel-exposed workers could be used as biomarkers of oxidative stress.

Plasma Lipid Peroxidation Zinc And Erythrocyte Cu-Zn Superoxide Dismutase Enzyme Activity In Patients With Type 2 Diabetes Mellitus In Gorgan City (South East Of The Caspian Sea)

The aim of this study was to determine the changes of plasma lipid peroxidation, zinc and erythrocyte Cu-Zn superoxide dismutase activity in patients with type 2 diabetes mellitus and healthy control in Gorgan city. Fifty type 2 patients with diabetes mellitus and 50 people without diabetes were included in this randomized study. None of patients studied had any diabetic complications. The levels of plasma malondialdehyde and zinc from type 2 diabetes mellitus patients (6.24±0.85 nmol mL-1 and 116.78±5.51 μ dL-1) and control groups (3.63±0.97 nmol mL-1 and 146.86±9.06 μg dL-1) were determined. Erythrocyte Cu-Zn superoxide dismutase activity from patients with diabetes (675.34±60.89 U g-1 Hb) and control groups (1052.70± 52.76 U g-1 Hb) were determined. The increased plasma lipid peroxidation and decreased plasma zinc and erythrocyte Cu-Zn superoxide dismutase activity that we observed in patients with type 2 diabetes mellitus may predispose to the development of cardiovascular complications. We propose that diabetic patients may have elevated requirement for antioxidants. Supplementation with zinc and vitamin or dietary free radical scavengers such as vitamins E and C or tomato, orange and etc. have a potential role in boosting antioxidant-related defences and maybe important in patients with diabetes.

Increased iron staining in the cerebral cortex of cholesterol fed rabbits

The link between hypercholesterolemia and neuronal damage is not clear. In the present study, we studied some of the possible effects of hypercholesterolemia on the brain, using the cholesterol fed New Zealand White rabbit as a model. An increase in the number of iron positive cells (i.e. oligodendrocytes) was observed in the brain parenchyma, in rabbits treated with a high cholesterol diet for 8 weeks. At this time, no neuronal death was observed, indicating that the increased iron did not occur as a consequence of neuronal injury. No heme oxygenase-1 (HO-1) or bilirubin immunoreactivity was observed in the brains in these rabbits, indicating that the iron accumulation did not occur as a consequence of increased breakdown of heme. It is postulated that cholesterol could have subtly damaged brain endothelial cells, resulting in increased iron transport across brain endothelial cells. Hypercholesterolaemia is known to be associated with increased plasma lipid peroxidation which might contribute to such damage.

Plasma lipid profile and lipid peroxidation in overweight or obese children and adolescents

To study the plasma lipid profile and lipid peroxidation in overweight or obese children and adolescents receiving care at the pediatric endocrinology clinic in HOSPED/UFRN, a university hospital. Three groups were studied: overweight (n = 15), obese (n = 30) and control (n = 21) children and adolescents. To evaluate plasma lipid profile, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglyceride levels were measured. Lipid peroxidation was determined by measuring malondialdehyde concentration. Data were analyzed using Student's t test, Tukey test, ANOVA and Pearson's correlation. Altered levels of total and LDL-cholesterol were observed mainly in overweight or obese males. HDL-cholesterol was borderline in the overweight and obese groups of both sexes. Obese females had the highest levels of triglycerides. Increased plasma lipid peroxidation was observed mainly in obese males. In the present population, the greatest alterations in lipid profile were observed in obese and overweight males. Plasma lipid peroxidation was more evident in obese males and females.

Enhanced inflammatory responses in α-tocopherol transfer protein null mice

The liver preferentially secretes α-tocopherol into plasma under the control of the hepatic α-tocopherol transfer protein (α-TTP). α-TTP-null mice ( Ttpa −/− mice) are vitamin E deficient, therefore were used for investigations of in vivo responses to sub-normal tissue α-tocopherol concentrations during inflammation. Increased basal oxidative stress in Ttpa −/− mice was documented by increased plasma lipid peroxidation, and superoxide production by bone marrow-derived neutrophils stimulated in vitro with phorbol 12-myristate 13-acetate. Lipopolysaccharide (LPS) injected intraperitoneally induced increases in lung and liver HO-1 and iNOS, as well as plasma NO x in Ttpa +/+ mice. LPS induced more modest increases in these markers in Ttpa −/− mice, while more marked increases in plasma IL-10 and lung lavage TNFα were observed. Taken together, these results demonstrate that α-tocopherol is important for proper modulation of inflammatory responses and that sub-optimal α-tocopherol concentrations may derange inflammatory–immune responses.

Effects of Ginkgo biloba extract on cytoprotective factors in rats with duodenal ulcer.

To investigate the effects of Ginkgo biloba extract on cytoprotective factors in rats with duodenal ulcer. Sprague-Dawley rats were randomly divided into four groups: sham operation without ginkgo, sham operation with ginkgo, duodenal ulcer without ginkgo, and duodenal ulcer with ginkgo. Rats with duodenal ulcer were induced by 500 mL/L acetic acid. Rats with ginkgo were intravenously injected with Ginkgo biloba extract from the tail at a dose of 0.5 mg/(kg/d) for 7 and 14 days. Pathological result showed that duodenal ulcer rats with ginkgo improved mucosal healing and inflammation compared with those without ginkgo after 7 d treatment. After 14 d treatment, duodenal ulcer rats with ginkgo significantly increased weight gain (34.0+/-4.5 g versus 24.5+/-9.5 g, P<0.05) compared with those without ginkgo. Duodenal ulcer rats significantly increased cell proliferation (27.4+/-4.0 and 27.8+/-2.3 BrdU-labeled cells in duodenal ulcer rats with and without ginkgo versus 22.4+/-3.5 and 20.8+/-0.5 BrdU-labeled cells in sham operation rats with and without ginkgo, P<0.05) compared with sham operation rats. Mucosal prostaglandin E(2) concentration significantly increased by 129% (P<0.05) in duodenal ulcer rats with ginkgo compared with that in those without ginkgo. Duodenal ulcer rats without ginkgo significantly decreased superoxide dismutase activity in the duodenal mucosa and erythrocytes (19.4+/-6.7 U/mg protein versus 38.1+/-18.9 U/mg protein in the duodenal mucosa, and 4.87+/-1.49 U/mg protein versus 7.78+/-2.16 U/mg protein in erythrocytes, P<0.05) compared with sham operation rats without ginkgo. However, duodenal ulcer rats with ginkgo significantly increased erythrocyte superoxide dismutase activity (8.22+/-1.92 U/mg protein versus 4.87+/-1.49 U/mg protein, P<0.05) compared with those without ginkgo. Duodenal ulcer rats without ginkgo significantly increased plasma lipid peroxides (4.18+/-1.12 micromol/mL versus 1.60+/-1.10 micromol/mL and 1.80+/-0.73 micromol/mL, P<0.05) compared with sham operation rats without ginkgo and duodenal ulcer rats with ginkgo during the experimental period. Ginkgo biloba extract can improve weight gain and mucosal healing in duodenal ulcer rats by the actions of cytoprotection and antioxidation.

Red blood cell membrane essential fatty acid metabolism in early psychotic patients following antipsychotic drug treatment

A role of indices of oxidative stress, oxidative injury, and abnormal membrane phospholipid, specifically the phospholipid essential polyunsaturated fatty acids (EPUFAs) metabolism has been suggested based on studies in separate groups of patients with or without medication. The current study investigated the relationship between these biochemical measures in first-episode psychotic patients ( N=16) at baseline and after 6 months of antipsychotic treatment ( N=5 each with risperidone and olanzapine) and compared them to matched normal subjects. The indices of oxidative stress included: antioxidant enzymes; superoxide dismutase, glutathione peroxidase and catalase; and the oxidative injury as the levels of plasma lipid peroxides. The key membrane EPUFA's been; linolenic acid, arachidonic acid, nervonic acid, docosapentaenoic acid and docosahexaenoic acid. Furthermore, the changes in these biochemical measures were correlated with clinical symptomatology. Data indicated that, at baseline, reduced levels of antioxidant enzymes were associated with increased plasma lipid peroxides and reduced membrane EPUFAs, particularly omega-3 fatty acids. Furthermore, these biochemical measures normalized after 6 months of antipsychotic treatment. Parallel-improved psychopathology indicated that membrane EPUFA status might be partly affected by oxidative damage, which together may contribute to the pathophysiology and thereby, psychopathology of schizophrenia. These data also support the augmentation of antipsychotic treatment by supplementation with a combination of antioxidants and omega-3 fatty acids.

Protective effect of sesamin administration on exercise-induced lipid peroxidation.

To investigate the mechanism of antioxidative effects of sesamin in vivo, 32 male ddY mice were administered with 10 mg/kg or 100 mg/kg of sesamin (S10, S100), 100 mg/kg of vitamin E (VE100) or control sample (C). They were subjected to 30 min of swimming exercise 2 h after the sample administration by using a new forced-swimming apparatus, i. e. an adjustable-current swimming pool. Exercise resulted in a significant increase in plasma lipid peroxides (LPO) in C and VE100 (p < 0.01), but not in S10 and S100. S100 showed significantly higher total glutathione peroxidase activity and glutathione S-transferase activity in liver compared to C (p < 0.05). In conclusion, sesamin may enhance LPO degradation in the liver resulting in the strong protective effects against exercise-induced plasma lipid peroxidation.

The effects of verbascoside on plasma lipid peroxidation level and erythrocyte membrane fluidity during immobilization in rabbits: a time course study

We studied the changes in the level of plasma lipid peroxidation indicated by malondialdehyde (MDA) level and erythrocyte membrane fluidity expressed by the value of order parameter (S) during single hindlimb immobilization of 21 days using thiobarbituric acid — reactive substances method and spin label electron spin resonance method, respectively. The impacts of verbascoside that has been proved its antioxidative activity on the measured parameters were examined. 11 New Zealand white rabbits were immobilized and divided into two groups. The rabbits in the verbascoside group were administrated with 0.8 mg/kg of verbascoside twice a day orally throughout the immobilization. The rabbits in the placebo group were treated with normal saline. In placebo group, the results showed that the level of MDA significantly increased on day 3, peaked on day 7, and was still significantly higher on day 14 of immobilization, compared with the value measured before immobilization. The value of S reached the highest on day 7 and subsequently lowered but still higher on day 14 than those measured before immobilization. Compared with placebo group, there were lower MDA level (P < 0.05, 0.001, and 0.05 for days 3, 7, and 14, respectively) and higher erythrocyte membrane fluidity (P < 0.05, 0.001, and 0.001 for days 3, 7, and 14, respectively) in verbascoside group. The data indicated that immobilization caused temporal changes of increase in plasma lipid peroxidation and decrease in erythrocyte membrane fluidity. Verbascoside might have the effects to moderate oxidative stress and erythrocyte membrane fluidity during immobilization.

Plasma susceptibility to free radical-induced antioxidant consumption and lipid peroxidation is increased in very old subjects with Alzheimer disease.

Oxidative stress is believed to play a major role in the pathogenesis of Alzheimer disease (AD). Plasma concentrations of vitamins C, A and E, of uric acid, thiols and carotenoids were lower and of malondialdehyde (MDA) higher in 35 AD patients (85.9 +/- 5.5 y) compared to 40 controls 85.5 +/- 4.4 y). Differences were significant for vitamin C, vitamin E, lutein, lycopene, alpha-carotene and MDA (p < 0.001). Plasma exposed to peroxyl radicals showed a rate of antioxidant consumption and of MDA production higher in AD patients than in controls. AD in advanced age is accompanied by a poor plasma antioxidant status and increased plasma lipid peroxidation, as well as by a low resistance to peroxyl radical exposure.

Vitamin C and E supplements improve the impaired antioxidant status and decrease plasma lipid peroxides in hemodialysis patients☆

This study investigated the supplementation with vitamin C or/and E on the antioxidant system in hemodialysis patients. Thirty-eight hemodialysis patients (27 males and 11 females) with the average of 60 years old were divided into four groups: placebo (400 mg starch/time), vitamin C (400 mg/time)-, vitamin E (400 mg d,l- α-tocopheryl acetate/time)-, and vitamin C (400 mg/time) + E (400 mg d,l- α-tocopheryl acetate/time)-supplemented groups for 6-week supplementation. The patients orally received three capsules of placebo or antioxidant(s) three times a week after finishing hemodialysis. Thirty-six healthy subjects (22 males and 14 females) with the average of 58 years old were recruited as the control group. Hemodialysis patients significantly decreased plasma vitamin C by 32%, erythrocyte glutathione by 26%, and plasma total antioxidant status by 9%, but increased plasma lipid peroxide levels by 102% compared with the control group at the baseline. The levels of plasma vitamin C and total antioxidant status significantly decreased by 24% and 18%, respectively, from the post-dialysate compared with those from the pre-dialysate. At week 6, vitamin C + E-supplemented group significantly increased plasma vitamin C and E, erythrocyte glutathione, and plasma antioxidant status, and inhibited plasma lipid peroxides compared with placebo group. Additionally, vitamin C + E-supplemented group had higher plasma vitamin C, vitamin E, and total antioxidant status, and lower plasma lipid peroxides than placebo group even at least 2 weeks after the termination of the supplements. Therefore, antioxidant vitamin supplements could improve antioxidant status and decrease lipid peroxides of hemodialysis patients.