The current study was conducted to investigate the ameliorative effect of moderate-intensity exercise training insole and simultaneous with insulin on diabetes (DM)-induced pathogenesis at the testicular tissue and sperm level. For this purpose, 36 mature male Wistar rats were divided into six groups, including sedentary control (Con), exercise training (EX), sedentary experimental DM-induced (SDM), exercise training + DM-induced (DM + EX), insulin-treated sedentary DM-induced (DM + INS) and exercise training and insulin-treated DM-induced (DM + INS + EX) groups. Following DM induction, the 6-week exercise training intervention (30 min of moderate-intensity running on a treadmill, once daily [5 days/week]) was considered in EX groups. The tubular differentiation (TDI) and spermiogenesis (SPI) indices, testicular total antioxidant capacity (TAC), superoxide dismutase (SOD) and glutathione peroxidase (GPX) contents, serum testosterone and insulin levels, the apoptosis ratio and sperm parameterswere assessed. The exercise in sole (EX) and simultaneous forms with INS (DM + INS + EX group) ameliorated the DM-suppressed spermatogenesis and spermiogenesis indices, up-regulated the serum testosterone and insulin levels, enhanced testicular SOD content, inhibited the apoptosis and improved almost all sperm parameters. In conclusion, exercise training, when simultaneously considered with insulin, fairly boosts the insulin-induced impacts, including the up-regulated testicular endocrine and antioxidant status, spermatogenesis and sperm quality.

Intravenous application of high-dose ascorbate (vitamin C) has been used in complementary medicine since the 1970s to treat cancer patients. In recent years it became evident that high-dose ascorbate in the millimolar range bears selective cytotoxic effects on cancer cells in vitro and in vivo. This anticancer effect is dose dependent, catalyzed by serum components and mediated by reactive oxygen species and ascorbyl radicals, making ascorbate a pro-oxidative pro-drug that catalyzes hydrogen peroxide production in tissues instead of acting as a radical scavenger. It further depends on HIF-1 signaling and oxygen pressure, and shows a strong epigenetic signature (alteration of DNA-methylation and induction of tumor-suppressing microRNAs in cancer cells). The detailed understanding of ascorbate-induced antiproliferative molecular mechanisms warrants in-depth preclinical evaluation in cancer-bearing animal models for the optimization of an efficacious therapy regimen (e.g., combination with hyperbaric oxygen or O2-sensitizers) that subsequently need to be evaluated in clinical trials.

More than 2000 species of edible and/or medicinal mushrooms have been identified to date, many of which are widely consumed, stimulating much research on their health-promoting properties. These properties are associated with bioactive compounds produced by the mushrooms, including polysaccharides. Althoughβ-glucans (homopolysaccharides) are believed to be the major bioactive polysaccharides of mushrooms, other types of mushroom polysaccharides (heteropolysaccharides) also possess biological properties. Here we survey the chemistry of such health-promoting polysaccharides and their reported antiobesity and antidiabetic properties as well as selected anticarcinogenic, antimicrobial, and antiviral effects that demonstrate their multiple health-promoting potential. The associated antioxidative, anti-inflammatory, and immunomodulating activities in fat cells, rodents, and humans are also discussed.The mechanisms of action involve the gut microbiota, meaning the polysaccharides act as prebiotics in the digestive system. Also covered here are the nutritional, functional food, clinical, and epidemiological studies designed to assess the health-promoting properties of polysaccharides, individually and as blended mixtures, against obesity, diabetes, cancer, and infectious diseases, and suggestions for further research. The collated information and suggested research needs might guide further studies needed for a better understanding of the health-promoting properties of mushroom polysaccharides and enhance their use to help prevent and treat human chronic diseases.

While mushrooms are the highest dietary source for the unique sulfur-containing antioxidant ergothioneine, little is known regarding levels of the major biological antioxidant glutathione. Thus, our objectives were to determine and compare levels of glutathione, as well as ergothioneine, in different species of mushrooms. Glutathione levels varied>20-fold (0.11-2.41mg/gdw) with some varieties having higher levels than reported for other foods. Ergothioneine levels also varied widely (0.15-7.27mg/gdw) and were highly correlated with those of glutathione (r=0.62, P<0.001). Both antioxidants were more concentrated in pileus than stipe tissues in selected mushrooms species. Agaricus bisporus harvested during the third cropping flush contained higher levels of ergothioneine and glutathione compared to the first flush, possibly as a response to increased oxidative stress. This study demonstrated that certain mushroom species are high in glutathione and ergothioneine and should be considered an excellent dietary source of these important antioxidants.

Oxidative stress causes the generation of reactive oxygen species (ROS) that lead to nephrotoxicity. An aminoglycoside, gentamicin, has pronounced nephrotoxic effect in humans and animals and this study was planned to observe the nephro-protective effect of antioxidants, vitamin C and Nigella sativa oil. Serum creatinine, blood urea nitrogen, and antioxidant activity were measured as indicators of nephrotoxicity for all the groups of rabbits. Results showed that vitamin C and Nigella sativa oil both had nephro-protective effect as they lowered the values of nephrotoxicity indicators (serum creatinine, blood urea nitrogen, and antioxidant activity) as compared to gentamicin control group values. When these two antioxidants were given as combination, they proved to have synergistic nephro-protective effect.

Nephrotoxicity induced by chlorpyrifos-ethyl (CE) and ameliorating effects of melatonin and vitamin E plus vitamin C were evaluated in rats exposed to CE. Experimental groups were as follows: control (C), CE treated (CE), vitamin E plus vitamin C treated (Vit), melatonin treated (Mel), vitamin E plus vitamin C plus CE treated (Vit+CE), and melatonin plus CE treated (Mel+CE). The rats in the CE, Vit+CE and Mel+CE groups were administered orally with CE in two equal doses of 41 mg/kg body weight (0.25 LD50). Melatonin and vitamins E and C were administrated intramuscularly at the doses of 10, 150 and 200 mg/kg, respectively. The levels of thiobarbituric acid reactive substance (TBARS) and antioxidant potential (AOP), and the activities of glutathione peroxidase (GSH-Px), catalase (CAT) and superoxide dismutase (SOD) were studied in the homogenates of kidney tissue. There were no significant differences in the activities of SOD and CAT between the experimental groups. The level of TBARS increased significantly (P<0.05) while AOP decreased significantly (P<0.05) in the CE group compared with the C group. GSH-Px activity was significantly (P<0.05) lower in the CE group and higher in the melatonin group than the control group. Histopathological changes were found in the kidney tissue of rats treated with CE. These were infiltration in mononuclear cells at perivascular and peritubular areas, hydropic degenerations in tubule epithelium and glomerular sclerosis. The severity of the lesions was reduced by administration of vitamins and melatonin. These results suggest that CE increases lipid peroxidation and decreases AOP by increasing oxidative stress, and that high doses of melatonin and a combination of vitamin E plus vitamin C considerably reduce the toxic effect of CE on kidney tissue of rats.

Ethanol induces oxidative stress and its exposure during early developmental age causes neuronal cell death which leads to several neurological disorders. We previously reported that vitamin C can protect against ethanol-induced apoptotic cell death in developing rat brain. Here, we extended our study to know the therapeutic efficacy of vitamin C against ethanol-induced oxidative stress, neuroinflammation mediated neurodegeneration in postnatal day 7 (PND7) rats. A single episode of ethanol (5g/kg) subcutaneous administration to PND7 rats significantly induced the production of reactive oxygen species (ROS), activation of both microglia and astrocytes followed by the induction of different apoptotic markers. On the other hand due to its free radical scavenging properties vitamin C treatment significantly reduced ROS production, suppressed both activated microglia and astrocytes and reversed other changes including elevated level of Bax/Bcl-2 ratio, cytochrome c and different caspases such as caspase-9 and caspase-3 induced by ethanol in developing rat brain. Moreover, vitamin C treatment also reduced ethanol-induced activation of PARP-1 and neurodegeneration as evident from Flouro-Jade-B and Nissl stainined neuronal cell death in PND7 rat brain. These findings suggest that vitamin C mitigated ethanol-induced oxidative stress, neuroinflammation and apoptotic neuronal loss and may be beneficial against ethanol abusing in brain development.

Accumulation of iron at sites where neurons degenerate in Parkinson's disease (PD) and Alzheimer's disease (AD) is thought to have a major role in oxidative stress induced process of neurodegeneration. The novel non-toxic lipophilic brain- permeable iron chelators, VK-28 (5- [4- (2- hydroxyethyl) piperazine-1-ylmethyl]- quinoline- 8- ol) and its multi-functional derivative, M-30 (5-[N-methyl-N-propargylaminomethyl]-8-hydroxyquinoline), as well as the main polyphenol constituent of green tea (-)-epigallocatechin-3-gallate (EGCG), which possesses iron metal chelating, radical scavenging and neuroprotective properties, offer potential therapeutic benefits for these diseases. M-30 and EGCG decreased apoptosis of human SH-SY5Y neuroblastoma cells in a neurorescue, serum deprivation model, via multiple protection mechanisms including: reduction of the pro-apoptotic proteins, Bad and Bax, reduction of apoptosis-associated Ser139 phosphorylated H2A.X and inhibition of the cleavage and activation of caspase-3. M-30 and EGCG also promoted morphological changes, resulting in axonal growth-associated protein-43 (GAP-43) implicating neuronal differentiation. Both compounds significantly reduced the levels of cellular holo-amyloid precursor protein (APP) in SH-SY5Y cells. The ability of theses novel iron chelators and EGCG to regulate APP are in line with the presence of an iron-responsive element (IRE) in the 5'-untranslated region (5'UTR) of APP. Also, EGCG reduced the levels of toxic amyloid-beta peptides in CHO cells over-expressing the APP"Swedish"mutation. The diverse molecular mechanisms and cell signaling pathways participating in the neuroprotective/neurorescue and APP regulation/processing actions of M-30 and EGCG, make these multifunctional compounds potential neuroprotective drugs for the treatment of neurodegenerative diseases, such as PD, AD, Huntington's disease and amyotrophic lateral sclerosis.

In previous studies, Nigella sativa (NS) has been studied due to its various physiological and pharmacological activities. However, evidence on the effects of NS on physical fatigue following exhaustive swimming remains limited. In the present study, the authors evaluated the potential beneficial effects of NS against the fatigue activity following exhaustive swimming. Rats were orally administered with NS extract (2 g/kg/day) for 21 days, and the anti-fatigue effect was assessed by exhaustive swimming exercise. The presented results indicated that pre-treatment of NS extract significantly increased the time to exhaustion. In hemodynamic parameters, NS extract increased blood pO2 and O2sat, but decreased pCO2. For underlying mechanisms, NS extract protected depletion of energy, indicated by increased levels of blood pH, glucose and tissue glycogen contents, and decreased levels of blood lactate, tissue lactic dehydrogenase and creatine kinase, when the NS extract was pre-treated. In addition, the NS extract inhibited oxidative stress following exhaustive swimming, as reflected by the results of increased levels of superoxide dismutase and redox ratio, and decreased the level of malondialdehyde when the NS extract was pre-treated. Collectively, the present study demonstrated that NS extract has an anti-fatigue activity against exhaustive swimming by energy restoration and oxidative-stress defense.

OBJECTIVE: To determine effects of oat and antioxidant vitamin (C 500 mg, E 400 IU) ingestion on endothelial function in overweight, dyslipidemic adults. DESIGN: Randomized, blinded, placebo-controlled, crossover trial Intervention(s): Subjects (16 males>or = age 35; 14 postmenopausal females) were assigned, in random order, to oats (60 g oatmeal), vitamin E (400 IU) plus vitamin C (500 mg), the combination of oats and vitamins, or placebo, and underwent brachial artery reactivity scans (BARS) following a single dose of each treatment, and again following 6 weeks of daily ingestion, with 2-week washout periods. At each test, a provocation high-fat meal (50 g, predominantly saturated) was administered and subjects were scanned pre, and 3 hours post-ingestion. RESULTS: Mean flow-mediated vasodilation (FMD; measured as percent diameter change before and after treatments) at baseline was 6.35 +/- 3.37. Oats increased FMD non-significantly (p>0.05) with both single acute dose (from 6.07 +/- 6.25 to 9.22 +/- 8.82) and six weeks of sustained treatment (from 6.01 +/- 10.07 to 8.69 +/- 8.42). The direction of effect was negative for vitamins and the oat/vitamin combination with both acute and sustained treatment. There were no significant differences in FMD change among the treatments in either phase of the study, however when acute and sustained effects were pooled, oat treatment significantly augmented FMD (p<0.05). CONCLUSIONS: This trial suggests but does not confirm a beneficial influence of oat ingestion on endothelial function in overweight, dyslipidemic adults. Further study of this potential association is warranted.

OBJECTIVE: Epidemiology suggests that Mediterranean diets are associated with reduced risk of cardiovascular disease. Because monocyte adhesion to the endothelium is crucial in early atherogenesis, we evaluated whether typical olive oil and red wine polyphenols affect endothelial-leukocyte adhesion molecule expression and monocyte adhesion.

METHODS AND RESULTS: Phytochemicals in olive oil and red wine, including oleuropein, hydroxytyrosol, tyrosol, elenolic acid, and resveratrol, with or without antioxidant activity, were incubated with human umbilical vein endothelial cells for 30 minutes, followed by co-incubation with bacterial lipopolysaccharide or cytokines to trigger adhesion molecule expression. At nutritionally relevant concentrations, only oleuropein, hydroxytyrosol, and resveratrol, possessing a marked antioxidant activity, reduced monocytoid cell adhesion to stimulated endothelium, as well as vascular cell adhesion molecule-1 (VCAM-1) mRNA and protein by Northern analysis and cell surface enzyme immunoassay. Reporter gene assays with deletional VCAM-1 promoter constructs indicated the relevance of nuclear factor-kappaB, activator protein-1, and possibly GATA binding sites in mediating VCAM-1 transcriptional inhibition. The involvement of nuclear factor-kappaB and activator protein-1 was finally demonstrated at electrophoretic mobility shift assays.

CONCLUSIONS: Olive oil and red wine antioxidant polyphenols at nutritionally relevant concentrations transcriptionally inhibit endothelial adhesion molecule expression, thus partially explaining atheroprotection from Mediterranean diets.

The clinical implications of non-alcoholic fatty liver diseases (NAFLD) derive from their potential to progress to fibrosis and cirrhosis. Inappropriate dietary fat intake, excessive intake of soft drinks, insulin resistance and increased oxidative stress results in increased free fatty acid delivery to the liver and increased hepatic triglyceride (TG) accumulation. An olive oil-rich diet decreases accumulation of TGs in the liver, improves postprandial TGs, glucose and glucagon-like peptide-1 responses in insulin-resistant subjects, and upregulates glucose transporter-2 expression in the liver. The principal mechanisms include: decreased nuclear factor-kappaB activation, decreased low-density lipoprotein oxidation, and improved insulin resistance by reduced production of inflammatory cytokines (tumor necrosis factor, interleukin-6) and improvement of jun N-terminal kinase-mediated phosphorylation of insulin receptor substrate-1. The beneficial effect of the Mediterranean diet is derived from monounsaturated fatty acids, mainly from olive oil. In this review, we describe the dietary sources of the monounsaturated fatty acids, the composition of olive oil, dietary fats and their relationship to insulin resistance and postprandial lipid and glucose responses in non-alcoholic steatohepatitis, clinical and experimental studies that assess the relationship between olive oil and NAFLD, and the mechanism by which olive oil ameliorates fatty liver, and we discuss future perspectives.

BACKGROUND:The effects of omega-3 polyunsaturated fatty acids (PUFA) on the prevention of postoperative atrial fibrillation (POAF) are inconclusive in current studies. Moreover, the most appropriate composition of PUFA to play the protective role is unclear. The aim of this meta-analysis was to ascertain the protective role of PUFA on POAF and the most appropriate composition.

METHODS:Studies were identified through PubMed, CENTRAL, EMBASE, reviews and reference lists of relevant papers. The odds ratio (OR) was calculated for POAF. Statistical analyses were performed with Review Manager 5.0.

RESULTS:Eleven randomised controlled trials with 3137 patients were included in the analysis. The use of PUFA alone did not reduce the incidence of POAF compared with the control (OR: 0.76; 95% confidence interval [CI]: 0.57-1.03; P=0.08; I(2)=52%). However, combination therapy with PUFA and vitamins C and E reduced the incidence of POAF by 68% (OR: 0.32; 95%CI: 0.17-0.60; P=0.0005; I(2)=38%). Subgroup analysis indicated that the ratio of EPA/DHA 1:2 was effective in preventing POAF (OR: 0.35; 95%CI: 0.24-0.50; P<0.00001; I(2)=0%), while the ratio not 1:2 failed.

CONCLUSIONS:Combination therapy with PUFA and vitamins C and E is effective in the prevention of POAF while PUFA alone is not. The ratio of EPA/DHA may influence the incidence of POAF, and 1:2 may be most appropriate. Studies about PUFA on the prevention of POAF are still worthwhile to be conducted in the future.

Nutrient levels in buckwheats that were maximized in day 8 sprouts (D8SP) included total phenolics, quercetin, and l-ascorbic acid, whereas those of oxalic, malic, tartaric, and citric acids, rutin, and gamma-aminobutyric acid (GABA) were found to reach maximum levels on day 10. Ethanolic extract of D8SP (2.5 mg/mL) revealed potent free-radical scavenging (FRS) and antioxidative (ANO) capabilities. However, its Fe2+-chelating capability was only moderate. To further study the hypolipidemic activity of D8SP, 36 Syrian hamsters were grouped into six groups and fed for 28 days, respectively, with (i) control meal, (ii) high fat plus high cholesterol meal, (iii) high fat plus high cholesterol plus 2.5% of buckwheat seeds, (iv) high fat plus high cholesterol plus 25% of buckwheat seeds, (v) high fat plus high cholesterol plus 2.5% of D8SP, and (vi) high fat plus high cholesterol plus 25% of D8SP. High seed meal prominently enhanced body weight gain, whereas high sprout meal exhibited the highest feed efficiency. Ratios of liver/body weight (L/B) were significantly lowered by all BS meals. Although low seed meal reduced serum total cholesterol (TC) levels (p<0.05), its effect was still inferior to the high seed and sprout meals (p<0.01). In contrast, serum triglyceride (TG) levels were lowered only by the high seed and sprout meals (p<0.05). Alternatively, levels of serum low-density lipoprotein cholesterol (LDL-C) were significantly suppressed by all buckwheat meals (p<0.01). Serum high-density lipoprotein cholesterol (HDL-C) levels were increased, however, insignificantly. Nutraceutically more meaningful is that both LDL-C/HDL-C and TC/HDL-C ratios were significantly lowered (p<0.01). Apparently, hepatic TC levels were significantly reduced, whereas hepatic TG levels were totally unaffected. Conclusively, sprouting triggers a variety of nutritional changes in buckwheats. Day 8 sprouts, consisting of high polyphenolic and moderate quercetin contents, are nutraceutically maximized when hypocholesterolemic, hypotriglyceridemic, and antioxidative activities are concerned.

BACKGROUND:Lead toxicity is a public health concern. Lead is one of the dispensable and non-biodegradable heavy metals and is toxic even at low concentrations.

OBJECTIVE:This study was to investigate the effect of oral administration of Vitamin C and Vitamin E on lead-induced hepatotoxicity and oxidative stress in the brain of rats.

METHODS:Thirty Sprague-Dawley albino male albino rats (115.58 +/- 4.96g) were divided equally into five groups. The rats were fed rat chow and water ad libitum. Group 1 rats served as control and were orally administered 2ml saline every day for 7 weeks. Group 2 rats received orally 2ml lead acetate solution (60mg/kg body weight) every day for 7 weeks. Group3 rats received orally 2ml lead acetate solution (60mg/kg body weight) and vitamin C (40mg/kg body weight) every other day for 7 weeks. Group 4 rats received orally 2ml lead acetate solution (60mg/kg body weight) and vitamin E (150mg/kg body weight)every day for 7weeks. Group 5 received orally lead acetate solution at 60mg/kg body weight and vitamin C (40mg/kg body weight)and vitamin E (150mg/kg body weight) every other day for 7weeks. Three rats from each group were sacrificed after the fourth week. The remaining rats were sacrificed after the seventh week. Changes in body weight, liver weight, brain weight, activities of liver function enzymes (aspartate amino transferase (AST), alanine amino transferase (ALT) and alkaline phosphatase(ALP) in the serum at week 4 and week 7 were assayed.The oxidative stress markers (reduced glutathione (GSH), nitric oxide(NO), malondialdehyde(MDA), levels, catalase(CAT) and superoxide dismutase (SOD) activities) were determined in the brain of rats. Serum lead level of rats was also determined.

RESULTS:The lead Pb exposed rats caused a significant (p<0.01) increase in bioavailable lead in the blood (p<0.05) as compared to the control. AST, ALT and ALPactivities were significantly increased (p<0.05) in the serum of rats exposed to lead as compared to the control. NO and MDA levels were significantly increased (p<0.05) in the brain of rats exposed to lead, while GSH level, SOD and CAT activities were significantly reduced (p<0.05) in the brain of rats exposed to lead when compared with the control.

CONCLUSION:Data of the study indicate that oral administration of vitamin C and vitamin E significantly reduced the blood lead concentration, ameliorates the hepatic damage and significantly reduced the oxidative stress in the brain of rats.

This study aims to compare the effect of early and late onset administration of oral antioxidants on number and quality of oocytes retrieved from aged mice after exogenous ovarian stimulation. Control hybrid females were fed a standard diet supplemented or not supplemented with pharmacological doses of vitamins C and E either from the first day of weaning or from the age of 32 weeks until they were autopsied at the age 40-42, 50-52, or 57-62 weeks after exogenous ovarian stimulation. Analysis of chromosomal distribution, DNA organization and cellular morphology was performed in ovulated cumulus-enclosed and -free oocytes, ovarian non-germinal vesicle oocytes enclosed by or free of mucous cumulus cells and in vitro-matured ovarian germinal-vesicle oocytes. Both early and late onset administration of oral antioxidants counteracted the negative effects of female aging on number of ovarian oocytes and total percentage of oocytes retrieved from oviducts and ovaries exhibiting a normal distribution of chromosomes in the metaphase-II plate and/or morphological traits of apoptosis. Although both early and late onset administration of oral antioxidants can counteract the negative effects of female aging on number and quality of oocytes, transference of these results to human beings should be made with caution because of the potential side effects of high doses of vitamins on reproductive function as well as many other undesirable systemic disorders.

AIM: This study aims to assess the antioxidant property of vitamins E and C in Helicobacter pylori infection, and to determine if adding them to standard triple therapy plus bismuth subcitrate increases the H. pylori eradication rate. METHODS: This study included 160 patients infected with H. pylori, who were randomized into one of two groups. Patients in group A (n = 80) received lansoprazole (30 mg, b.i.d.), amoxicillin (1000 mg, b.i.d.), clarithromycin (500 mg, b.i.d.), and bismuth subcitrate (300 mg, q.i.d.) for 14 days, while patients in group B (n = 80) received vitamin C (500 mg, b.i.d.) and vitamin E (200 IU, b.i.d.) for 30 days, in addition to lansoprazole (30 mg, b.i.d.), amoxicillin (1000 mg, b.i.d.), clarithromycin (500 mg, b.i.d.), and bismuth subcitrate (300 mg, q.i.d.) for 14 days. Total antioxidant capacity (TAC) was evaluated with a Randox kit. Success rate was calculated using both intention-to-treat (ITT) and per-protocol (PP) analyses. RESULTS: One hundred and sixty patients were analyzed using ITT analysis. One hundred and fifty-three patients completed the study. In group A, H. pylori eradication was achieved in 48 (60%) of the 80 patients included in the ITT analysis, and in 48 (64%) of the 75 patients included in the PP analysis. In group B, H. pylori eradication was achieved in 73 (91.25%) of the 80 included in the ITT analysis and in 73 (93.5%) of the 78 patients included in the PP analysis. The eradication rate was significantly higher in group B than in group A (p<.005). TAC was at the lower limit of normal in both groups and the difference between them was not statistically significant (p>.05). CONCLUSION: In group B, H. pylori eradication rate was 91.25%, which is higher than the ideal 80% eradication rate. The results of the present study show that adding the prescribed doses of vitamins E and C to antimicrobial therapy is effective in eradicating H. pylori infection.

BACKGROUND: Previous studies have shown that urogenital tuberculosis (GuTb) patients treated or untreated with regular anti-Tb regimen excrete comparatively high levels of urinary stone forming constituents than normal subjects. Enhanced oxidative stress is also considered as a prime factor that accelerates urolithiasis. The present study was aimed to determine antioxidant status and lipid peroxidation of these individuals in order to assess their risk for kidney stone formation. METHODS: GuTb patients and age-matched normal subjects were divided into four groups: I: normal subjects (n=60), II: GuTb patients a day before treatment (n=72), III: GuTb patients after treatment with isoniazid (300 mg), rifampicin (450 mg) and pyrazinamide (1.5 g) per day for 60 days (n=42), and IV: GuTb patients supplemented with vitamin E (200 mg/day) along with regular chemotherapy for 60 days (n=30). Blood was collected and tested for various markers of oxidative stress. RESULTS: Increased levels of lipid peroxidation, protein carbonyls (PCO), advanced oxidative protein products (AOPP) and reduced antioxidant defenses by impairment in enzyme activities like superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione and decreased plasma concentrations of non enzymatic antioxidants like vitamins C and E were observed in the treated and untreated GuTb patients. CONCLUSIONS: These biochemical disparities may lead to membrane disintegrity, which is favorable for retention of mirolithis. Advocation of vitamin E enhanced the antioxidant status of the plasma, thereby preventing membrane injury, consequently reducing the risk of stone formation in urogenital tuberculosis patients, who were treated with their routine anti-tuberculosis drug regimen.

The aim of the present study was to determine the effects of Nigella sativa (NS) oil concurrent with a low-calorie diet on lipid peroxidation and oxidative status in obese women. In this double-blind placebo-controlled randomized clinical trial, 50 volunteer obese (body mass index = 30-35 kg/m(2) ) women aged 25-50 years old were recruited. Participants were randomly divided into intervention (n = 25) and placebo (n = 25) groups. They received a low-calorie diet with 3 g/day NS oil or low-calorie diet with 3 g/day placebo for 8 weeks. Forty-nine women (intervention group = 25; placebo group = 24) completed the trial. NS oil concurrent with a low-calorie diet decreased weight in the NS group compared to the placebo group (-4.80 ± 1.50 vs. -1.40 ± 1.90 kg; p < 0.01). Comparison of red blood cell superoxidase dismutase (SOD) indicated significant changes in the NS group compared to the placebo group at the end of the study (88.98 ± 87.46 vs. -3.30 ± 109.80 U/gHb; p < 0.01). But no significant changes in lipid peroxidation, glutathione peroxidase, and total antioxidant capacity concentrations were observed. NS oil concurrent with a low-calorie diet decreased weight and increased SOD levels in obese women. However, more studies are suggested to confirm the positive effects of NS in obesity and its complications. Copyright © 2015 John Wiley&Sons, Ltd.

Oxidative stress in the central nervous system (CNS) may cause oxidation of lipoprotein particles. The oxidized lipoproteins may damage cellular and subcellular membranes, leading to tissue injury and cell death. Human low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) are oxidized by transition metal ions, such as Cu2+. Using PC 12 cells, we tested the cytotoxicity of oxidized LDL and VLDL. Cell death was increased in a dose-dependent manner. Antioxidants added to the incubation medium, such as vitamins E or C, or resveratrol showed some protection. Results indicated that oxidized lipoproteins may serve as an oxidative stressor, which may initiate the neuronal cell death leading to the manifestation of Alzheimer disease (AD).