Increased Plasma Lipid Peroxidation Research Articles

Oxidative stress–induced fibrinogen modifications in liver transplant recipients: unraveling a novel potential mechanism for cardiovascular risk

BackgroundCardiovascular events represent a major cause of non–graft-related death after liver transplant. Evidence suggest that chronic inflammation associated with a remarkable oxidative stress in the presence of endothelial dysfunction and procoagulant environment plays a major role in the promotion of thrombosis. However, the underlying molecular mechanisms are not completely understood. ObjectivesIn order to elucidate the mechanisms of posttransplant thrombosis, the aim of the present study was to investigate the role of oxidation-induced structural and functional fibrinogen modifications in liver transplant recipients. MethodsA case-control study was conducted on 40 clinically stable liver transplant recipients and 40 age-matched, sex-matched, and risk factor–matched controls. Leukocyte reactive oxygen species (ROS) production, lipid peroxidation, glutathione content, plasma antioxidant capacity, fibrinogen oxidation, and fibrinogen structural and functional features were compared between patients and controls. ResultsPatients displayed enhanced leukocyte ROS production and an increased plasma lipid peroxidation with a reduced total antioxidant capacity compared with controls. This systemic oxidative stress was associated with fibrinogen oxidation with fibrinogen structural alterations. Thrombin-catalyzed fibrin polymerization and fibrin resistance to plasmin-induced lysis were significantly altered in patients compared with controls. Moreover, steatotic graft and smoking habit were associated with high fibrin degradation rate. ConclusionROS-induced fibrinogen structural changes might increase the risk of thrombosis in liver transplant recipients.

Anti-atherogenic role of green tea (Camellia sinensis) in South Indian smokers

Ethnopharmacological relevanceGreen tea (Camellia sinensis) is a popular beverage consumed all over the world due to its health benefits. Many of these beneficial effects of green tea are attributed to polyphenols, particularly catechins. Aim of the studyThe present study focuses on underlying anti-platelet aggregation, anti-thrombotic, and anti-lipidemic molecular mechanisms of green tea in South Indian smokers. Materials and methods: We selected 120 South Indian male volunteers for this study to collect the blood and categorised them into four groups; control group individuals (Controls), smokers, healthy control individuals consuming green tea, and smokers consuming green tea. Smokers group subjects have been smoking an average 16–18 cigarettes per day for the last 7 years or more. The subjects (green tea consumed groups) consumed 100 mL of green tea each time, thrice a day for a one-year period. ResultsLC-MS analysis revealed the presence of multiple phytocompounds along with catechins in green tea extract. Increased plasma lipid peroxidation (LPO), protein carbonyls, cholesterol, triglycerides, and LDL-cholesterol with decreased HDL-cholesterol levels were observed in smokers compared to the control group and the consumption of green tea showed beneficial effect. Furthermore, docking studies revealed that natural compounds of green tea had high binding capacity with 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA) when compared to their positive controls, whereas (−) epigallocatechin-3-gallate (EGCG) and (−) epicatechin-gallate (ECG) had high binding capacity with sterol regulatory element-binding transcription factor 1 (SREBP1c). Further, our ex vivo studies showed that green tea extract (GTE) significantly inhibited platelet aggregation and increased thrombolytic activity in a dose dependent manner. ConclusionIn conclusion, in smokers, catechins synergistically lowered oxidative stress, platelet aggregation and modified the aberrant lipid profile. Furthermore, molecular docking studies supported green tea catechins' antihyperlipidemic efficacy through strong inhibitory activity on HMG-CoA reductase and SREBP1c. The mitigating effects of green tea on cardiovascular disease risk factors in smokers that have been reported can be attributed majorly to catechins or to their synergistic effects.

ROS-driven structural and functional fibrinogen modifications are reverted by interleukin-6 inhibition in Giant Cell Arteritis

BackgroundCranial and extra-cranial vascular events are among the major determinants of morbidity and mortality in Giant Cell Arteritis (GCA). Vascular events seem mostly of inflammatory nature, although the precise pathogenetic mechanisms are still unclear. We investigated the role of oxidation-induced structural and functional fibrinogen modifications in GCA. The effects of the anti-IL6R tocilizumab in counteracting these mechanisms were also assessed. Materials and methodsA cross-sectional study was conducted on 65 GCA patients and 65 matched controls. Leucocyte reactive oxygen species (ROS) production, redox state, and fibrinogen structural and functional features were compared between patients and controls. In 19 patients receiving tocilizumab, pre vs post treatment variations were assessed. ResultsGCA patients displayed enhanced blood lymphocyte, monocyte and neutrophil ROS production compared to controls, with an increased plasma lipid peroxidation and a reduced total antioxidant capacity. This oxidative impairment resulted in a sustained fibrinogen oxidation (i.e. dityrosine content 320 (204–410) vs 136 (120–176) Relative Fluorescence Units (RFU), p < 0.0001), with marked alterations in fibrinogen secondary and tertiary structure [intrinsic fluorescence: 134 (101–227) vs 400 (366–433) RFU, p < 0.001]. Structural alterations paralleled a remarkable fibrinogen functional impairment, with a reduced ability to polymerize into fibrin and a lower fibrin susceptibility to plasmin-induced lysis. In patients receiving tocilizumab, a significant improvement in redox status was observed, accompanied by a significant improvement in fibrinogen structural and functional features (p < 0.001). ConclusionsAn impaired redox status accounts for structural and functional fibrinogen modifications in GCA, suggesting a potential role of tocilizumab for cardiovascular prevention in GCA.

Lipid composition and oxidative changes in diabetes and alcoholic diabetes rats

BackgroundThe investigating of study was expected to the lipid composition of diabetes and alcoholic diabetes in plasma and erythrocyte membrane biochemical profile in rats. Diabetic male Wistar Streptozotocin (STZ)-induced rats were used experimental models. Control rats (C) were maintained group I, received glucose (i.e., caloric equivalent), diabetic induced rats (STZ) group II, and group III alcoholic treated and IV diabetic and alcoholic treated rats which received 20 % (v/v) alcohol in water, administered through stomach tube (5 g/kg body weight/day). ResultsSTZ-induced diabetic hepatic damage in rats was observed which leads to the increased plasma lipid peroxidation, nitrate and nitrite levels. Diabetic and administration alcohol rats also suggestively lesser the activities of antioxidants, glutathione peroxidase, glutathione S-transferase, superoxide dismutase, catalase and reduced glutathione when related with control rats (group I). Plasma enzymes are normal levels and renovate the enzymic and non-enzymatic antioxidants level in experimental groups. ConclusionThe present data point out that the nitric oxide scavenging levels increased and may possibly protect and adjacent to oxidative stress and free radicals in diabetic hepatopathy rats and histopathological studies were identified in regular hepatic cortex of Group II, III and IV of animals with diabetes, alcoholic and alcohol-induced diabetes rats.

Effect of Resistance Training With Total and Partial Blood Flow Restriction on Biomarkers of Oxidative Stress and Apoptosis in Untrained Men.

Introduction: The characterization of immune and oxidative stress responses to acute and chronic exercise training is important because it may aid in the safety and dose–response prescription of resistance training (RT) in many populations.Purpose: The present study compared changes in acute oxidative stress and markers of apoptosis in immune cells before and after 8 weeks of low-load RT with total or partial blood flow restriction (BFR) versus high-load traditional RT.Methods: Twenty-seven untrained men were randomly divided into three groups: traditional RT [75% one-repetition maximum (1-RM)], RT with partial (20% 1-RM), and total BFR (20% 1-RM). Over an 8-week period, participants performed six sets of arm curls until failure with 90 seconds of recovery for 3 days/week. Blood samples were obtained before and after the first and last training sessions.Results: Data indicated that all training groups showed similar increases in muscular strength (p < 0.001), reduction in mitochondrial membrane potential (MMP) after exercise in neutrophils (p < 0.001), and increase in caspase-3 activity after exercise (p < 0.001). Traditional RT and total BFR showed increased plasma lipid peroxidation (p < 0.001) and protein carbonyls (p < 0.001) and lower levels of reduced glutathione (GSH) (p < 0.001) after exercise. No change was observed in oxidative stress biomarkers in response to partial BFR (p > 0.05).Conclusion: Data show that RT with partial BFR can increase muscular strength but still does not augment biomarkers of oxidative stress in untrained men. In addition, RT with total BFR promoted similar responses of oxidative stress and markers of immune cell apoptosis versus traditional RT.

Effects of plant-derived isoquinoline alkaloids on growth performance and intestinal function of broiler chickens under heat stress

Broiler chickens reared under heat stress (HS) conditions have decreased growth performance and show metabolic and immunologic alterations. This study aimed to evaluate the effect of supplementation with a standardized blend of plant-derived isoquinoline alkaloids (IQ) on the growth performance, protein catabolism, intestinal barrier function, and inflammatory status of HS-treated chickens. Three hundred sixty 0-day-old Ross 308 male broiler chickens were randomly distributed into 2 treatment groups: control diet (no additives) or diet supplemented with 100 ppm IQ. At day 14, the chicks in each diet group were further divided into 2 groups, each of which was reared under thermoneutral (TN) (22.4°C) or constant HS (33.0°C) conditions until day 42. Each group consisted of 6 replicates with 15 birds per replicate, and chickens were provided ad libitum access to water and feed. During days 15–21, the body weight gain (BWG) and feed intake (FI) were significantly lower in the HS treatment group than in the TN group, and feed conversion ratio was higher (P < 0.05); these factors were not alleviated by IQ supplementation. During days 22–42, the final BW, BWG, and FI of the HS birds were better among those administered IQ than those that were not (P < 0.05). HS treatment increased plasma lipid peroxide, corticosterone, and uric acid concentrations as well as serum fluorescein isothiocyanate–dextran, a marker of intestinal barrier function, and decreased plasma total protein content (P < 0.05). These changes were not observed in the IQ group, suggesting that IQ supplementation improved oxidative damage, protein catabolism, and intestinal barrier function of chickens under HS. Isoquinoline alkaloid supplementation inhibited the expression of intestinal inflammatory factors, IL-6, tumor necrosis factor–like factor 1A, and inducible nitric oxide synthase under HS treatment (P < 0.05). These results suggest that IQ supplementation can improve the growth performance of broiler chickens under HS conditions, which may be associated with amelioration of oxidative damage, protein catabolism, intestinal barrier function, and inflammation.

Leptin Replacement Therapy Improves Endothelial Function and Vascular Inflammation in a Mouse Model of Acquired Lipodystrophy Associated with Antiretroviral Treatment by Regulating Nox1‐Derived ROS and C‐C Chemokine Receptor Type 5

Highly active antiretroviral therapy (HAART) has been used at suppressing HIV replication, as a side effect HAART promotes lipodystrophy, which is a metabolic disorder characterized by an abnormal adipose tissue distribution, reduced leptin plasma levels and vascular complications. Leptin replacement therapy (LRT) is currently used to treat metabolic dysfunctions in patients diagnosed with congenital lipodystrophy. Here, we sought to investigate whether LRT restores vascular function and reduces inflammation in mice treated with the antiretroviral agent, ritonavir. Four weeks of ritonavir reduced body weight [control (C): 28.4±0.5 vs. Rit: 24.4 ± 0.2g*, *P&lt;0.05], fat mass (C: 10 ± 0.4 vs. Rit: 4.5 ± 0.9 %*, *P&lt;0.05) and leptin plasma levels (C: 4.7 ± 0.05 vs. Rit: 2.0 ± 0.36 ng/mL*, *P&lt;0.05) confirming that it induces acquired lipodystrophy. Acquired lipodystrophy impaired endothelial function, increased plasma lipid peroxidation and vascular H2O2, and ROS producing enzymes (Nox1 and NoxA1). Furthermore, acquired lipodystrophy was associated with vascular inflammation characterized by elevation of NLRP3, Caspase‐1, IL‐1β, MCP‐1, F4/80, CCR5 and CCL5 gene expression. ROS scavenging via tempol (SOD mimetic, 100 μmol/l) or GKT771 (Nox1 inhibitor, 10 μmol/l) restored endothelial function. LRT (10μg/day/7 days, osmotic mini‐pump), at the end of the 3‐week ritonavir, restored endothelial function, reduced vascular oxidative stress and Nox1 and NOXA1 gene expression and vascular inflammation. Nox1 deficiency (Nox1−/−) protected mice from acquired lipodystrophy‐induced endothelial dysfunction and reduced inflammatory markers including CCR5 and CCL5. In order to analyze whether vascular inflammation is occurring via CCR5/CCL5, we induced lipodystrophy in CCR5 deficient mice (CCR5−/−). These mice were protected from acquired lipodystrophy‐induced endothelial dysfunction and vascular inflammation. Moreover, deleting endothelial leptin signaling via specific deletion of leptin receptor (LepR) in endothelial cells (LepR−/−EC mice) promoted endothelial dysfunction, which was reverted by pre‐incubating aortic rings with Nox1 inhibitor (GKT771) in vitro and increased inflammatory markers. Furthermore, LepR−/−EC mice were resistant to the vascular protective effects of LRT. Taken all together, LRT restores endothelial function and reduces vascular inflammation in acquired lipodystrophy associated with HAART via endothelium dependent reduction in Nox1‐derived ROS and CCR5/CCL5. Taken together these data support a key role for endothelial leptin signaling in the control of vascular tone and inflammation and suggest that LRT could represent a potential new avenue for the treatment of vascular diseases associated with acquired lipodystrophy.Support or Funding InformationWork supported by 17POST33410363 and 1K99HL140139‐01A1 to TBN and 1R01HL13030101 to EJ.BdC.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Obesity: an independent risk factor for oxidative stress

Background: Obesity is increasing in prevalence and presents a serious risk for the development of various disorders like diabetes mellitus, hypertension, heart disease, gall bladder disease and certain forms of cancer. Animal studies have shown that obesity is associated with increased myocardial oxidative stress and increased lipid peroxidation. The objective of this study was to test the hypothesis that obesity per se causes increased plasma lipid peroxidation and decreased erythrocyte cytoprotection.Methods: A prospective randomized study including 300 obese subjects, was conducted in the Department of Medicine and Department of Biochemistry, G. R. Medical College, Gwalior. Age and sex matched 100 subjects having BMI between 19 to 25 kg/m2 were also enrolled. Patients were grouped as Case (n=300) and Control (n=100). Detailed physical examination and laboratory investigations including lipid profile were performed. Venous blood was obtained and used for the estimation of Superoxide dismutase (SOD) and plasma malondialdehyde (MDA). Unpaired t test and analysis of variance (ANOVA) with post-hoc Bonferroni and Tukey test along with Pearson correlation was used to analyze the data using IMB SPSS ver. 20 software. Significance is assessed at 5 % level.Results: Mean age of subjects among Case and Control group was 46.2±2.4 years and 44.5±2.2 years respectively with male predominance in each group. Mean weight, height, BMI, waist, hip, waist to hip ratio, mean blood glucose, total cholesterol, triglyceride, LDL-C, HDL-C and VLDL-C among Cases were91.57±9.8 kg, 161.6±9.3 cm, 36.17± 3.4 kgm2, 114.7±6.2 cm, 114.23±17.12 cm, 0.98±0.22, 87.3±2.6 mg/dl, 196.0±12.6 mg/dl, 253.6±27.3 mg/dl, 135±47.03 mg/dl, 47.1±1.2 mg/dl and 45.8±14.03 mg/dl and among Control group were61±5.2 kg, 163.1±8.7 cm, 21.24±1.88 cm, 21.24±1.88 kg m2, 85.2±1.4 cm, 97.32±9.12 cm, 0.86±0.14, 94.4 ± 3.2 mg/dl, 186.6 ± 6.9 mg/dl, 143.4±15.4 mg/dl, 95.73±27.48 mg/dl, 51.6±1.7 mg/dl and 22.4±10.45mg/dl respectively. Mean MDA level in Case and Control group was 4.68 ± 1.72 and 2.06±0.76 μmol/ml respectively (p&lt; 0.001). Mean SOD level among Case and Control groups was 7.65±1.13 and 12.42±2.18 units/ml respectively (p&lt;0.001). Female obese patients had lower level of SOD. A significant negative correlation of SOD was observed with BMI (n=300, r= -0.045, P&lt;0.001), whereas, MDA was positively correlated with BMI (n=300, r= 0.342, P&lt;0.001).Conclusions: Obesity in humans is an independent risk factor for lipid peroxidation and depletion of cytoprotective enzymes even in the absence of other confounding factors such as diabetes and hyperlipidaemia.

Nitric oxide and oxidative stress is associated with severity of diabetic retinopathy and retinal structural alterations.

The aim of the study was to determine plasma nitric oxide (NO) and lipid peroxide (LPO) levels in diabetic retinopathy and its association with severity of disease. Prospective observational study. A total of 60 consecutive cases and 20 healthy controls were included. Severity of retinopathy was graded according to early treatment diabetic retinopathy study (ETDRS) classification. Photoreceptor inner segment ellipsoid band (ISel) disruption and retinal pigment epithelium (RPE) alteration were graded using spectral domain optical coherence tomography. Data were statistically analyzed. Plasma thiobarbituric acid reactive substances, NO assay and reduced glutathione (GSH) were measured using standard protocol. Increased severity of diabetic retinopathy was significantly associated with increase in plasma levels of LPO (P < 0.05), NO (P < 0.001) and decrease in plasma levels of GSH (P < 0.0001), ISel disruption (P < 0.001) and RPE topographic alteration (P < 0.01). Increased plasma NO levels are associated with increased severity of diabetic retinopathy. For the first time, it has been demonstrated that increased plasma LPO, NO and decreased GSH levels are associated with in vivo structural changes in inner segment ellipsoid and RPE.

Application of FTIR-ATR Spectroscopy to Determine the Extent of Lipid Peroxidation in Plasma during Haemodialysis.

During a haemodialysis (HD), because of the contact of blood with the surface of the dialyser, the immune system becomes activated and reactive oxygen species (ROS) are released into plasma. Particularly exposed to the ROS are lipids and proteins contained in plasma, which undergo peroxidation. The main breakdown product of oxidized lipids is the malondialdehyde (MDA). A common method for measuring the concentration of MDA is a thiobarbituric acid reactive substances (TBARS) method. Despite the formation of MDA in plasma during HD, its concentration decreases because it is removed from the blood in the dialyser. Therefore, this research proposes the Fourier Transform Infrared Attenuated Total Reflectance (FTIR-ATR) spectroscopy, which enables determination of primary peroxidation products. We examined the influence of the amount of hydrogen peroxide added to lipid suspension that was earlier extracted from plasma specimen on lipid peroxidation with use of TBARS and FTIR-ATR methods. Linear correlation between these methods was shown. The proposed method was effective during the evaluation of changes in the extent of lipid peroxidation in plasma during a haemodialysis in sheep. A measurement using the FTIR-ATR showed an increase in plasma lipid peroxidation after 15 and 240 minutes of treatment, while the TBARS concentration was respectively lower.

Effects of Dietary Chrysin Supplementation on Blood Pressure and Oxidative Status of Rats Fed a High-Fat High-Sucrose Diet

Effects of dietary chrysin supplementation on blood pressure and oxidative status of rats were studied in comparison with quercetin. Rats were fed a control diet or a high-fat high-sucrose (HFS) diet with or without 0.25% flavonoids (chrysin or quercetin) for 4 weeks. In rats fed the HFS diet without flavonoids, there was a significant elevation of blood pressure, increase in aortic NADPH oxidase but not xanthine oxidase, an increase in plasma lipid peroxides, and a decrease in liver glutathione, compared to rats fed the control diet. Chrysin suppressed the elevation of blood pressure in rats fed the HFS diets at the same level as quercetin. Chrysin supplementation did not suppress the increase in NADPH oxidase activity and plasma lipid peroxides or the decrease in liver glutathione, whereas these effects were significant with quercetin. Also, the results of an in vitro experiment suggested that chrysin did not exert antioxidative effects on lipid peroxidation in a linoleic acid emulsion. These results suggest that chrysin has an antihypertensive effect similar to quercetin, but unlike quercetin is not antioxidative in normotensive rats fed a HFS diet. Thus, it is probable that a mechanism(s) other than antioxidative activity is responsible for the suppression of hypertension by chrysin.

Diosmin exhibits anti-hyperlipidemic effects in isoproterenol induced myocardial infarcted rats

The aim of the present study was to evaluate the protective effects of diosmin on experimentally induced myocardial infarcted rats. Diosmin (5 and 10mg/kg body weight) was administered orally as pretreatment daily for a period of 10 days. Then isoproterenol (100mg/kg) was injected subcutaneously into rats at an interval of 24h for 2 days (on 11th and 12th day). Isoproterenol-induced myocardial infarcted rats showed significant changes in electrocardiogram and an increase in the levels of cardiac markers, compared with normal rats. Additionally, increased plasma lipid peroxidation products and altered lipid metabolism in the plasma were observed in the isoproterenol-induced myocardial infarcted rats. Pretreatment with diosmin (5 and 10mg/kg body weight) minimized the electrocardiographic changes, decreased the levels of serum cardiac marker enzymes reduced plasma lipid peroxidation and minimized the alterations in the lipid metabolism of isoproterenol-induced myocardial infarcted rats. Also, diosmin inhibited the enhanced activity of liver HMG CoA reductase. The in vitro study revealed the free radical scavenging activity of diosmin. The free radical scavenging and anti-hyperlipidaemic effects are the reasons for the cardioprotective effects of diosmin.

The Effects of Ziprasidone, Clozapine and Haloperidol on Lipid Peroxidation in Human Plasma (in vitro): Comparison

Oxidative injury in schizophrenia can be caused by the disease itself and probably by antipsychotics treatment. The aim of the study was to establish whether there is a difference between ziprasidone, clozapine and haloperidol effect on lipid peroxidation in human plasma, measured by the level of thiobarbituric acid reactive substances (TBARS). The samples of plasma from healthy subjects were incubated with the drugs (1 and 24 h) and compared with control samples. The levels of TBARS were measured spectrophotometrically, according to the Rice-Evans method. The multifactorial variance analysis ANOVA II test showed that the differences in TBARS levels significantly depended on the studied drugs (ziprasidone 40 ng/ml, haloperidol 4 ng/ml and clozapine 350 ng/ml) (F = 3.248 p = 0.047) and (ziprasidone 139 ng/ml, haloperidol 20 ng/ml and clozapine 420 ng/ml) (F = 2.248, p = 2.9 × 10(-5)). Statistically increased levels of TBARS after 24 h incubation of plasma with ziprasidone 139 ng/ml and haloperidol 20 ng/ml (p < 0.001, p < 0.05 respectively) in comparison with control samples were observed. Clozapine did not significantly (p > 0.05) increase TBARS level in plasma in comparison with control samples. The results obtained in the study showed that ziprasidone and haloperidol contrary to clozapine induced a significant increase in plasma lipid peroxidation.

Effect of Lutein on L-NAME-Induced Hypertensive Rats

We investigated the antihypertensive effect of lutein on NG-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats. Daily oral administration of L-NAME (40 mg/kg)-induced a rapid progressive increase in mean arterial pressure (MAP). L-NAME significantly increased MAP from the first week compared to that in the control and reached 193.3±9.6 mmHg at the end of treatment. MAP in the lutein groups was dose-dependently lower than that in the L-NAME group. Similar results were observed for systolic and diastolic blood pressure of L-NAME-induced hypertensive rats. The control group showed little change in heart rate for 3 weeks, whereas L-NAME significantly reduced heart rate from 434±26 to 376±33 beats/min. Lutein (2 mg/kg) significantly prevented the reduced heart rate induced by L-NAME. L-NAME caused hypertrophy of heart and kidney, and increased plasma lipid peroxidation four-fold but significantly reduced plasma nitrite and glutathione concentrations, which were significantly prevented by lutein in a dose-dependent manner. These findings suggest that lutein affords significant antihypertensive and antioxidant effects against L-NAME-induced hypertension in rats.

Protective effects of N‐acetyl cysteine on membrane‐bound adenosine triphosphatases and minerals in isoproterenol‐induced myocardial‐infarcted rats: An in vivo and in vitro study

The present study was aimed to evaluate the protective effects of N-acetyl cysteine (NAC) on changes in the activities/levels of adenosine triphosphatases and minerals in isoproterenol-induced myocardial-infarcted rats. Male albino Wistar rats were pretreated with NAC (10 mg/kg body weight) daily for a period of 14 days. After pretreatment period, rats were induced myocardial infarction (MI) by isoproterenol (100 mg/kg body weight). The activity of sodium/potassium-dependent adenosine triphosphatase was decreased, and the activities of calcium- and magnesium-dependent adenosine triphosphatases were increased in the heart of isoproterenol-induced myocardial-infarcted rats. Furthermore, the levels of potassium were lowered and the levels of sodium and calcium were increased in the heart of isoproterenol-induced rats. Increased plasma lipid peroxidation was observed in isoproterenol-induced rats. Pretreatment with NAC showed protective effects on adenosine triphosphatases, minerals, and lipid peroxidation. The in vitro study confirmed the reducing property of NAC. The observed effects are due to the membrane-stabilizing and antioxidant effects of NAC. The results of this study will be useful for the prevention of MI.

Lipid Peroxidation in Judoists Using Oral Contraceptives

12 female judoists using oral contraceptives (OCU) containing 0.03 mg ethinylestradiol and 3 mg drospirenone for 20 ± 12 months (mean ± SD) were compared with a control group of 14 judoist noncontraceptive users (NCU) in order to evaluate resting (T1) and postexercise (T2) lipid peroxidation (LPO) and antioxidant parameters. Data were collected 20 min before and 10 min after a morning session of judo training and included determination of lag phase (Lp) before free radical-induced oxidation, glutathione peroxidase (GPx), α-tocopherol, retinol, and oxidative stress markers related to LPO. Significantly higher resting oxidative stress (+125.8 and +165.2% for malondialdehyde and lipid peroxides, respectively) and lower values of Lp and GPx (-23.4 and -12.1%, respectively) were observed in the OCU compared with NCU. The judo training session induced an increase in plasma LPO whatever the treatment. We noted significant increases in Lp (+14.7%; p<0.05 vs. preexercise) and GPx (22.1%; p<0.05 vs. preexercise) only in the NCU group. We suggest that a judo training session favourably altered some antioxidants in NCU but not in OCU. As excessive oxidative stress is linked to the development of several chronic diseases, the use of agents to reduce antioxidants may be reasonable in OCU.

Assessment of oxidative stress in lymphocytes with exercise

This study investigated whether changes in the cellular composition of blood during exercise could partly account for observations of exercise-induced changes in lymphocyte oxidative stress markers. Markers of oxidative stress were assessed before and after 60 min of intense treadmill running. Samples were collected from 16 men (means ± SD: age 33 ± 13 yr; body mass index 23.8 ± 2.5 kg/m(2); maximal oxygen uptake 59.7 ± 5.2 ml·kg(-1)·min(-1)). Peripheral blood lymphocytes were assayed for protein carbonyl concentration, and plasma was assessed for lipid peroxides and antioxidant capacity. In a separate study, intracellular thiol concentration was determined in lymphocyte subsets from eight characteristically similar men by flow cytometry, of which T-cell memory populations were further identified on the basis of CD27, CD28, and CD45RA expression. Total lymphocyte protein carbonyls were transiently increased with exercise and returned to baseline within 15 min (P < 0.001). This change was accompanied by an increase in plasma lipid peroxides (P < 0.05) and total antioxidant capacity (P < 0.001). Correlation analyses showed that lymphocyte protein carbonyl content was not related to changes in the cellular composition of peripheral blood during exercise. Natural killer cells (CD3(-)CD56(+)) and late-differentiated/effector memory cells (CD4(+)/CD8(+)CD27(-)CD28(-)/CD45RA(+)), which mobilized most with exercise, showed high intracellular thiol content (P < 0.001). High thiol content suggests a lower oxidative load carried by these lymphocytes. Thus vigorous exercise resulted in a transient increase in lymphocyte oxidative stress. Results suggest this was unrelated to the alterations in the cellular composition of peripheral blood.

Evidence for Improved Neuropharmacological Efficacy and Decreased Neurotoxicity in Mice with Traditional Processing ofRhizoma Arisaematis

Rhizoma Arisaematis (RA, the rhizome of Pinellia pedatisecta Schott) is a traditional Chinese medicine commonly used in the treatment of convulsions, inflammation, and cancer. Despite the fact that it has been used for more than 2000 years, the pharmacological and toxic effects of traditionally processed products of RA are still unclear. In this study, we attempted to investigate the effects exerted by untreated crude RA and different preparations of RA treated with alumen in combination with ginger juice (Zhinanxing) or bile juice (Dannanxing) in ICR mice. The results showed that both the Zhinanxing and Dannanxing water extracts exerted significantly increased sedative effects, as indicated by the inhibitory effects on ambulatory distances, jumps, vertical-plane entries, and prolonged pentobarbital-induced sleeping time. The extracts also exerted significantly increased analgesic effects (increase of tail flick latency in nociceptive testing) in mice than did the unprocessed crude RA after oral administration for one to three days, and effects persisted 18 days after the cessation of treatment. By contrast, the toxic effects, such as an increase in stereotype-1 episodes of locomotor activities and reduction of the retention time on a rotating rod (motor equilibrium dysfunction), were observed only in mice treated with the unprocessed crude RA for three consecutive days, and effects persisted for 18 days after the cessation of treatment. These neurotoxic effects were accompanied by an increase in plasma lipid peroxidation (LPO), decrease in whole blood nitric oxide (NO(x)) levels, and inhibition of Na(+)/K(+)-ATPase activities in membrane fractions of erythrocytes and in the cerebral cortex. In conclusion, these findings provide scientific evidence that the processed RA indeed possesses not only enhanced neuropharmacological efficacy but also reduced neurotoxic effects as compared to the unprocessed crude RA. The signaling of NO(x)/oxidative stress/Na(+)-K(+)- ATPase activities played a role, at least in part, in the underlying mechanisms of neurotoxic effects induced by the crude RA.

Lipid Peroxidation Alterations in Type 2 Diabetic Patients

It was studied that type 2 diabetes mellitus is connected with increased plasma lipid peroxidation (lipid peroxidation expressed as malondialdehyde). This review aimed to evaluate the state of lipid peroxidation among type 2 diabetic subjects. Present finding showed that lipid peroxidation increased in type 2 diabetes mellitus. Increased lipid peroxidation maybe is associated with some diseases such as cancer, cardiovascular diseases and diabetes mellitus. Lipid peroxidation has an important role in the pathogenesis and the complications of diabetes. Antioxidants have been found to prevent the progression and occurrence of diabetes. There are several mechanisms that may cause lipid peroxidation affront in diabetic subjects, although, their precise contributions are not completely clear. We proposed that production of free radicals can be reduced by preventing high blood glucose levels and by the control of instabilities in blood glucose levels. A contributor to these instabilities in blood glucose is glycaemic control by using of fast blood sugar test. Furthermore, the earlier assessment of the advancement of diabetes that firmly control of blood glucose can be obtained; the greater will be the decrease in diabetic complications. Patients with type 2 diabetes may have very high physiological antioxidants requirements.

Ghrelin, Nitrite and Paraoxonase/Arylesterase Concentrations in Cement Plant Workers

Ghrelin, Nitrite and Paraoxonase/Arylesterase Concentrations in Cement Plant WorkersOccupational cement dust exposure has been associated with an increased risk of liver abnormalities, pulmonary disorders, and carcinogenesis. Decreased antioxidant capacity and increased plasma lipid peroxidation have been posed as possible causal mechanisms of disease. Accordingly, this study examined the serum paraoxonase (PON1) arylesterase (AE), ghrelin, HDL-C, LDL-C and serum nitrite (NOx) levels in cement dust exposed workers. Twenty-eight volunteer male cement plant workers and 30 volunteer control male workers, aged 29-54 years, participated. The concentrations of serum PON1, AE, NOx, ghrelin, and HDL-cholesterol and LDL-cholesterol were measured in both groups. PON-1, AE, ghrelin and HDL-cholesterol were lower in the cement plant workers than in controls. Serum nitrite (NOx), and LDL-C levels in cement plant workers were higher (p&lt;0.05) than in the control group workers. No correlation was observed between the serum levels of HDL-cholesterol and PON1 and between HDL-cholesterol and ghrelin. A weak negative correlation was detected between the serum ghrelin and NOx. The study results strongly suggest that HDL-paraoxonase, AE, ghrelin, HDL-C, and high NOx, and LDL-C levels may have a role in disease involving oxidative damage. However, some studies are necessary to address the association between occupational dust exposure and respiratory symptoms.