F2-isoprostane Levels Research Articles

Tick-borne encephalitis – lipid peroxidation and its consequences

Background: The purpose of this study was to assess the processes of lipid peroxidation with prostaglandin derivatives and reactive aldehydes being its major indicators in cerebrospinal fluid (CSF), plasma and urine of patients with tick-borne encephalitis (TBE). Materials and methods: This study included 60 patients with TBE and 56 healthy subjects. Lipid peroxidation was estimated by the measurement of 4-hydroxynonenal (4-HNE), 4-hydroxyhexenal (4-HHE), malondialdehyde (MDA), acrolein, crotonaldehyde, and 4-oxononenal (4-ONE), determined by GC-MS, F2-isoprostanes and neuroprostanes (NPs) level determined by LC-MS. The level of 4-HNE-protein adducts was determined by ELISA. Phospholipase A2 (PLA2), platelet-activating factor acetylhydrolase (PAF-AH) and glutathione peroxidase (GSH-Px) activities and vitamin E level were determined spectrophotometrically and by HPLC, respectively. In parallel, the plasma levels of phospholipid acids such as arachidonic acid (AA), linoleic acid (LA) and docosahexaenoic acid (DHA) were monitored. Results: A significant decrease in AA, LA, DHA level and GSH-Px activity (by about 20, 69, 11 and 18%, respectively) was observed. The consequence of enhanced phospholipid peroxidation was almost 7 times higher plasma level of F2-isoprostanes and 3-fold increase in NPs level in CSF of TBE patients. Additionally a 3.5-fold increase in the CSF level of MDA, 5-fold increase in the plasma level of 4-HNE and urine level of 4-HHE in TBE patients was observed. Decreased plasma activity of PLA2 with an increase in the PAF-AH activity was observed. Conclusion: Lipid peroxidation occurring during TBE development indicates its relevance in pathophysiology of this disease. Moreover lipid peroxidation products might be useful for the diagnosis of TBE.

Levels of F2-isoprostanes, F4-neuroprostanes, and total nitrate/nitrite in plasma and cerebrospinal fluid of patients with traumatic brain injury

Several events occurring during the secondary damage of traumatic brain injury (TBI) can cause oxidative stress. F2-isoprostanes (F2-IsoPs) and F4-neuroprostanes (F4-NPs) are specific lipid peroxidation markers generated from arachidonic acid and docosahexaenoic acid, respectively. In this study, we evaluated oxidative stress in patients with moderate and severe TBI. Since sedatives are routinely used to treat TBI patients and propofol has been considered an antioxidant, TBI patients were randomly treated with propofol or midazolam for 72 h postoperation. We postoperatively collected cerebrospinal fluid (CSF) and plasma from 15 TBI patients for 6–10 d and a single specimen of CSF or plasma from 11 controls. Compared with the controls, the TBI patients exhibited elevated levels of F2-IsoPs and F4-NPs in CSF throughout the postsurgery period regardless of the sedative used. Compared with the group of patients who received midazolam, those who received propofol exhibited markedly augmented levels of plasma F2-IsoPs, which were associated with higher F4-NPs levels and lower total nitrate/nitrite levels in CSF early in the postsurgery period. Furthermore, the higher CSF F2-IsoPs levels correlated with 6-month and 12-month worse outcomes, which were graded according to the Glasgow Outcome Scale. The results demonstrate enhanced oxidative damage in the brain of TBI patients and the association of higher CSF levels of F2-IsoPs with a poor outcome. Moreover, propofol treatment might promote lipid peroxidation in the circulation, despite possibly suppressing nitric oxide or peroxynitrite levels in CSF, because of the increased loading of the lipid components from the propofol infusion.

Abstract 1889: Paleolithic and Mediterranean diet pattern scores and their associations with biomarkers of inflammation and oxidative balance

Abstract Chronic inflammation is associated with poor diet quality as well as risk for cancer and other chronic diseases. A diet-inflammation association may relate to evolutionary discordance. We investigated associations of two diet pattern scores, the “Paleolithic” and the Mediterranean, with circulating levels of two inflammation-related biomarkers, C-reactive protein (CRP), an acute inflammatory protein, and F2-isoprostanes, a reliable marker of lipid peroxidation in vivo, in a colonoscopy-based, pooled case-control study of incident sporadic colorectal adenomas (N = 646). We created diet scores from responses on a modified Willett food-frequency questionnaire, and measured plasma levels of CRP and F2-isoprostanes by ELISA and GCMS, respectively. Both diet scores were calculated and categorized into quintiles, and their associations with the biomarker levels were estimated using unconditional logistic regression. The multivariable-adjusted odds ratios (OR) comparing those in the highest relative to those in the lowest quintiles of the Paleolithic and Mediterranean diet scores, were, respectively, 0.73 (95% confidence interval [CI] 0.39, 1.36; Ptrend = 0.35) and 0.71 (95% CI 0.36, 1.40; Ptrend = 0.12) for CRP levels, and 0.35 (95% CI 0.17, 0.74; Ptrend <0.01) and 0.64 (95% CI 0.29, 1.40; Ptrend = 0.03) for F2-isoprostanes levels. These findings, which are particularly strong for the inverse Paleolithic diet score-F2-isoprostanes association, suggest that diets that are more “Paleolithic-” or Mediterranean-like may be associated with lower levels of systemic inflammation and oxidative stress. Citation Format: Kristine Whalen, Marji McCullough, W. Dana Flanders, Terryl J. Hartman, Suzanne Judd, Roberd M. Bostick. Paleolithic and Mediterranean diet pattern scores and their associations with biomarkers of inflammation and oxidative balance. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1889. doi:10.1158/1538-7445.AM2015-1889

Regular Yoga Practice Improves Antioxidant Status, Immune Function, and Stress Hormone Releases in Young Healthy People: A Randomized, Double-Blind, Controlled Pilot Study.

The aim of the present study is to highlight the beneficial effects of yoga practice on bio-parameters, such as oxidative stress, antioxidant components, immune functions, and secretion of stress hormones, in healthy young people. This study was conducted on healthy volunteers recruited from among university students, who were divided into two groups: a control (no yoga intervention, n=13) group and a yoga (n=12) group. Yoga practice was with an instructor for 90 minutes once a week spread over 12 weeks, with recommendations to practice daily at home for 40 minutes with the help of a DVD. The yoga program consisted of yoga body poses (asanas), exercises involving awareness, voluntary regulation of breath (pranayama), and meditational practices. Whole blood samples were collected when the volunteers had fasted for 8 hours at 0 and 12 weeks. The oxidative stress/antioxidant components, immune-related cytokines, and stress hormones were evaluated in serum or plasma. Serum levels of nitric oxide, F2-isoprostane, and lipid peroxide were significantly decreased by yoga practice (p<0.05 or p=0.01), whereas serum total glutathione (GSH) contents, activities of GSH-peroxidase, and GSH-s-transferase were remarkably increased after yoga practice compared with the control group (p<0.05 or p=0.01). Yoga practice also significantly increased immune-related cytokines, such as interleukin-12, and interferon-γ, in serum (p<0.05 or p=0.01). Yoga practice significantly reduced the plasma levels of adrenalin (p<0.05) and increased plasma levels of serotonin compared with the control group (p<0.05). Regular yoga practice remarkably attenuated oxidative stress and improved antioxidant levels of the body. Moreover, yoga beneficially affected stress hormone releases as well as partially improved immune function.

Exercise training attenuates sympathetic activation and oxidative stress in diet-induced obesity.

It is known that excessive sympathetic activity and oxidative stress are enhanced in obesity. This study aimed to clarify whether exercise training (ET) attenuates sympathetic activation and oxidative stress in obesity. The obesity was induced by high-fat diet (HFD) for 12 weeks. Male Sprague-Dawley rats were assigned to four groups: regular diet (RD) plus sedentary (RD-S), RD plus ET (RD-ET), HFD plus sedentary (HFD-S), and HFD plus ET (HFD-ET). The rats in RD-ET and HFD-ET groups were trained on a motorized treadmill for 60 min/day, five days/week for 8 weeks. The sympathetic activity was evaluated by the plasma norepinephrine (NE) level. The superoxide anion, malondialdehyde and F2-isoprostanes levels in serum and muscles were measured to evaluate oxidative stress. The ET prevented the increases in the body weight, arterial pressure and white adipose tissue mass in HFD rats. The NE level in plasma and oxidative stress related parameters got lower in HFD-ET group compared with HFD-S group. We have found decreased mRNA and protein levels of toll-like receptor (TLR)-2 and TLR-4 by ET in HFD rats. These findings suggest that ET may be effective for attenuating sympathetic activation and oxidative stress in diet-induced obesity.

Reduction in oxidative stress biomarkers after adenotonsillectomy

ObjectivesA number of otolaryngic conditions such as chronic tonsillitis, adenoid hypertrophy, and obstructive sleep apnea are associated with oxidative stress and elevated levels of serum oxidants. The objective of this study is to measure changes in urine biomarkers of oxidative stress in children after adenotonsillectomy. MethodsTwenty-two children with sleep disordered breathing (SDB) with tonsil and adenoid hypertrophy were enrolled prior to adenotonsillectomy. Controls consisted of 20 healthy children. Urine samples were collected from all patients. Levels of three urinary biomarkers for oxidative status, 8-hydroxy-2-deoxyguanosine (8-OxodG), F2-isoprostane, and malondialdehyde (MDA) were measured using high performance liquid chromatography. For the study group, urine samples were repeated 3 weeks after surgery. ResultsIn the study group, preoperative urinary levels of 8-OxodG were higher than in controls (p=0.015). Levels decreased after surgery compared to preoperative levels (p=0.002), and reached control levels (p=0.167) at 3 weeks. Levels of urinary F2-isoprostane were similar in both groups (p=0.252), but decreased significantly after surgery (p=0.020). ConclusionsChildren with SDB have elevated levels of urinary 8-OxodG, a marker of oxidative stress. Adenotonsillectomy results in decreased 8-OxodG and F2-isoprostane. These findings suggest that urine analysis may represent a valuable tool for the measurement of oxidative stress.

Uric acid correlates to oxidation and inflammation in opposite directions in women

Objective: To evaluate the association of uric acid (UA) levels with a panel of markers of oxidative stress and inflammation.Methods: Plasma UA levels, along with a panel of oxidative stress and inflammatory markers, were measured in 755 Chinese women.Results: Plasma UA levels were inversely associated with urinary levels of the oxidative stress marker F2-isoprostanes and positively correlated to levels of inflammatory markers, such as C-reactive protein and some proinflammatory cytokines (tumor necrosis factor-α and interleukin-6) in blood as well as prostaglandin E2 metabolites in urine.Conclusions: Plasma UA levels correlate to oxidation and inflammation biomarkers in opposite directions in women.

P47phox contributes to albuminuria and kidney fibrosis in mice

Reactive oxygen species (ROS) play an important pathogenic role in the development of many diseases, including kidney disease. Major ROS generators in the glomerulus of the kidney are the p47phox-containing NAPDH oxidases NOX1 and NOX2. The cytosolic p47phox subunit is a key regulator of the assembly and function of NOX1 and NOX2 and its expression and phosphorylation are up-regulated in the course of renal injury, and have been shown to exacerbate diabetic nephropathy. However, its role in non-diabetic-mediated glomerular injury is unclear. To address this, we subjected p47phox-null mice to either adriamycin-mediated or partial renal ablation-mediated glomerular injury. Deletion of p47phox protected the mice from albuminuria and glomerulosclerosis in both injury models. Integrin α1-null mice develop more severe glomerulosclerosis than wild type mice in response to glomerular injury mainly due to increased production of ROS. Interestingly, the protective effects of p47phox knockout were more profound in p47phox/integrin α1 double knockout mice. In vitro analysis of primary mesangial cells showed that deletion of p47phox led to reduced basal levels of superoxide and collagen IV production. Thus, p47phox-dependent NADPH oxidases are a major glomerular source of ROS, contribute to kidney injury, and are potential targets for antioxidant therapy in fibrotic disease.

The effect of mild traumatic brain injury on peripheral nervous system pathology in wild-type mice and the G93A mutant mouse model of motor neuron disease

Traumatic brain injury (TBI) is associated with a risk of neurodegenerative disease. Some suggest a link between TBI and motor neuron disease (MND), including amyotrophic lateral sclerosis (ALS). To investigate the potential mechanisms linking TBI to MND, we measured motor function and neuropathology following mild-TBI in wild-type and a transgenic model of ALS, G93A mutant mice. Mild-TBI did not alter the lifespan of G93A mice or age of onset; however, rotarod performance was impaired in G93A verses wild-type mice. Grip strength was reduced only in G93A mice after mild-TBI. Increased electromyography (EMG) abnormalities and markers of denervation (AchR, Runx1) indicate that mild-TBI may result in peripheral effects that are exaggerated in G93A mice. Markers of inflammation (cell edema, astrogliosis and microgliosis) were detected at 24 and 72h in the brain and spinal cord in wild-type and G93A mice. Levels of F2-isoprostanes, a marker of oxidative stress, were increased in the spinal cord 24h post mild-TBI in wild-type mice but were not affected by TBI in G93A mice. In summary, our data demonstrate that mild-TBI induces inflammation and oxidative stress and negatively impacts muscle denervation and motor performance, suggesting mild-TBI can potentiate motor neuron pathology and influence the development of MND in mice.

Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype

Our previous studies showed that adult (8 month) mice lacking CuZn-superoxide dismutase (CuZnSOD, Sod1KO mice) have neuromuscular changes resulting in dramatic accelerated muscle atrophy and weakness that mimics age-related sarcopenia. We have further shown that loss of CuZnSOD targeted to skeletal muscle alone results in only mild weakness and no muscle atrophy. In this study, we targeted deletion of CuZnSOD specifically to neurons (nSod1KO mice) and determined the effect on muscle mass and weakness. The nSod1KO mice show a significant loss of CuZnSOD activity and protein level in brain and spinal cord but not in muscle tissue. The masses of the gastrocnemius, tibialis anterior and extensor digitorum longus (EDL) muscles were not reduced in nSod1KO compared to wild type mice, even at 20 months of age, although the quadriceps and soleus muscles showed small but statistically significant reductions in mass in the nSod1KO mice. Maximum isometric specific force was reduced by 8–10% in the gastrocnemius and EDL muscle of nSod1KO mice, while soleus was not affected. Muscle mitochondrial ROS generation and oxidative stress measured by levels of reactive oxygen/nitrogen species (RONS) regulatory enzymes, protein nitration and F2-isoprostane levels were not increased in muscle from the nSod1KO mice. Although we did not find evidence of denervation in the nSod1KO mice, neuromuscular junction morphology was altered and the expression of genes associated with denervation acetylcholine receptor subunit alpha (AChRα), the transcription factor, Runx1 and GADD45α) was increased, supporting a role for neuronal loss of CuZnSOD initiating alterations at the neuromuscular junction. These results and our previous studies support the concept that CuZnSOD deficits in either the motor neuron or muscle alone are not sufficient to initiate a full sarcopenic phenotype and that deficits in both tissues are required to recapitulate the loss of muscle observed in Sod1KO mice.

Levels of F2 isoprostane in Behcet's disease: Correlation with cardiometabolic risk factors

ObjectiveBehcet's disease (BD) is a chronic inflammatory disease and recent findings suggest a role of oxidative stress in the pathogenesis of BD. Free radical-induced oxidative stress is also involved in the pathogenesis of cardiovascular and other rheumatic diseases. Oxidative stress may be detected in vivo by measuring F2 isoprostanes. Here, we measured plasma levels of F2 isoprostane in patients with BD and evaluated the correlation of F2 isoprostane with cardiometabolic risk factors.MethodsForty-three patients with BD in remission and 37 age- and sex-matched controls were recruited for the study. Blood samples were obtained to determine F2 isoprostane, C-reactive protein levels, erythrocyte sedimentation rate, and other biochemical parameters. Homeostasis model assessment insulin resistance and body mass index were calculated. Systolic blood pressure, diastolic blood pressure, and waist circumference were measured.ResultsPlasma F2 isoprostane, fasting plasma glucose, triglyceride, and C-reactive protein levels were significantly higher in patients with BD compared with healthy controls, whereas high-density lipoprotein cholesterol levels were significantly lower in patients with BD. F2 isoprostane levels did not correlate with cardiometabolic risk factors, C-reactive protein levels, or erythrocyte sedimentation rate.ConclusionHigh levels of F2 isoprostane in patients with BD indicate oxidative stress. Antioxidant therapeutic approaches could potentially affect the course of this disease.

Multiple Sclerosis: Effect of Oral Administration of an Antioxidant Dietary Supplement in C57BL6/N Induced Model of Experimental Autoimmune Encephalomyelitis

In the pathogenesis of demyelinating diseases including multiple sclerosis (MS) an important role is played by oxidative stress. Increased energy requirements during remyelination of axons and mitochondria failure is one of the causes of axonal degeneration and disability in MS. In the presence of neurological diseases such as MS, F2-isoprostanes are concentrated in higher quantities. In this context, we analyzed the levels of F2-isoprostanes in the plasma and cerebrospinal fluid of mice of the strain C57BL6/N with an induced experimental autoimmune encephalomyelitis (EAE), orally treated with two concentrations of Citozym, a dietary supplement with evident antioxidant properties. Compared to the control group, Citozym-treated EAE-mouse had significantly lower levels of F2-isoprostanes both in plasma and in cerebrospinal fluid. Furthermore, according to the guidelines of IACUC, treatment with Citozym at higher concentrations drastically reduced neurological signs of induced EAE.

Chilean Strawberry Consumption Protects against LPS-Induced Liver Injury by Anti-Inflammatory and Antioxidant Capability in Sprague-Dawley Rats.

The Chilean strawberry fruit has high content of antioxidants and polyphenols. Previous studies evidenced antioxidant properties by in vitro methods. However, the antioxidant effect and its impact as functional food on animal health have not been evaluated. In this study, rats were fed with a Chilean strawberry aqueous extract (4 g/kg of animal per day) and then subjected to LPS-induced liver injury (5 mg/kg). Transaminases and histological studies revealed a reduction in liver injury in rats fed with strawberry aqueous extract compared with the control group. Additionally, white strawberry supplementation significantly reduced the serum levels and gene expression of TNF-α, IL-6, and IL-1β cytokines compared with nonsupplemented rats. The level of F2-isoprostanes and GSH/GSSG indicated a reduction in liver oxidative stress by the consumption of strawberry aqueous extract. Altogether, the evidence suggests that dietary supplementation of rats with a Chilean white strawberry aqueous extract favours the normalization of oxidative and inflammatory responses after a liver injury induced by LPS.

New risk factors for adult-onset incident asthma. A nested case-control study of host antioxidant defense.

Host antioxidant defense, consisting of enzymatic antioxidant activity and nonenzymatic antioxidant micronutrients, is implicated in asthma pathogenesis. Studies of antioxidant defense and adult incident asthma have either used measures of antioxidants estimated from questionnaires or not considered enzymatic aspects of host defense. We conducted the first study designed and powered to investigate the association of antioxidant defenses on adult incident asthma. In a nested case-control study, we followed Shanghai women (aged 40-70 years) without prevalent asthma at baseline, over 8 years. Subjects with incident asthma were ascertained prospectively by gold standard testing of symptomatic women and matched to two asymptomatic control subjects. Baseline urinary F2-isoprostanes, plasma concentrations of antioxidant micronutrients (tocopherols, xanthines, carotenes, and lycopene), and antioxidant enzyme activity (platelet-activating factor acetylhydrolase [PAF-AH] and superoxide dismutase) were measured from samples collected before disease onset. Among 65,372 women, 150 (0.24%) developed asthma. F2-isoprostane levels before asthma onset were not different between cases and control subjects. Doubling of α-tocopherol concentrations and PAF-AH activity was associated with 50 and 37% decreased risk of incident asthma (α-tocopherol: adjusted odds ratio = 0.52; 95% confidence interval, 0.32-0.84; PAF-AH: adjusted odds ratio = 0.63; 95% confidence interval, 0.42-0.93). In this prospective study, α-tocopherol, within normal reference ranges, and PAF-AH enzymatic activity were associated with decreased asthma development. These modifiable risk factors may be an effective strategy to test for primary asthma prevention.

Moderate oral supplementation with docosahexaenoic acid improves platelet function and oxidative stress in type 2 diabetic patients.

Platelets from patients with type 2 diabetes are characterised by hyperactivation and high level of oxidative stress. Docosahexaenoic acid (DHA) may have beneficial effects on platelet reactivity and redox status. We investigated whether moderate DHA supplementation, given as a triglyceride form, may correct platelet dysfunction and redox imbalance in patients with type 2 diabetes. We conducted a randomised, double-blind, placebo-controlled, two-period crossover trial (n=11 post-menopausal women with type 2 diabetes) to test the effects of 400 mg/day of DHA intake for two weeks on platelet aggregation, markers of arachidonic acid metabolism, lipid peroxidation status, and lipid composition. Each two week-period was separated from the other by a six-week washout. Daily moderate dose DHA supplementation resulted in reduced platelet aggregation induced by collagen (-46.5 %, p< 0.001), and decreased platelet thromboxane B2 (-35 %, p< 0.001), urinary 11-dehydro-thromboxane B2 (-13.2 %, p< 0.001) and F2-isoprostane levels (-19.6 %, p< 0.001) associated with a significant increase of plasma and platelet vitamin E concentrations (+20 % and +11.8 %, respectively, p< 0.001). The proportions of DHA increased both in plasma lipids and in platelet phospholipids. After placebo treatment, there was no effect on any parameters tested. Our findings support a significant beneficial effect of low intake of DHA on platelet function and a favourable role in reducing oxidative stress associated with diabetes.

Novel Associations of F2-Isoprostanes, F3- Isoprostanes and Isofurans in Older Adults with Chronic Fatigue Syndrome: An Exploratory Study

Plasma levels of F2-isoprostanes (F2-IsoPs), a whole body oxidative stress marker, have been noted to be elevated in populations with chronic fatigue syndrome (CFS). We hypothesized that the oxidative stress biomarkers of F2-isoprostanes (F2-IsoPs), isofurans (IsoFs) and F3-isoprostanes (F3-IsoPs) are related to hypothalamic-pituitary-adrenal (HPA) axis dysregulation in chronic fatigue syndrome (CFS) subjects assessed by plasma dehydroepiandrosterone (DHEA) and cortisol and gene expression of sirtulin-1 (SIRT1). Plasma samples were obtained from nine CFS individuals aged 65 years or older. The mean levels of plasma F2-IsoPs (M=178 pg/ml, SD=100) and IsoFs (M=266 pg/ml, SD=205) were several-fold higher than previously reported in healthy subjects. F2-IsoPs:F3-IsoPs and SIRT1 were negatively associated (r=– .674, p<.05) whereas F3-IsoPs were inversely correlated with DHEA (r=– .586, p<.05) and positively associated with SIRT1 (r=.733, p<.05). After correction for age and sex, the F2-IsoPs:IsoFs ratio was positively correlated to DHEA:cortisol (r=.758, p<.05).The findings indicate that plasma IsoFs and F2-IsoPs are elevated in older subjects with CFS and that isoprostane and isofuran ratios are associated with HPA dysregulation.

Habitual high intake of fatty fish is related to lower levels of F2-isoprostane in healthy women

ObjectiveThe aim of this study was to determine whether habitual dietary intake of fatty fish, whole grains, fruits and vegetables, or a combination of them all, is associated with oxidative stress levels, measured as urine concentration of 8-iso-prostaglandin F2α (8-iso-PGF2α) in healthy women. MethodsEighty-one participants were included in this cross-sectional study. Mean age of the women was 26.1 ± 6.2 (mean ± SD) years and mean body mass index (BMI) was 22.4 ± 3.0 kg/m2. The concentration of 8-iso-PGF2α was determined in urine, and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) levels were determined in blood. Participants' habitual fish, whole grain, fruit, and vegetable intake was estimated from a food frequency questionnaire. ResultsIn the multivariate analysis, there was a significant inverse association between 8-iso-PGF2α and high fatty fish intake (P < 0.001). Fatty fish intake was positively correlated to serum phospholipid concentrations of EPA (P = 0.001) and DHA (P = 0.002). A borderline effect of DHA was seen on 8-iso-PGF2α, but higher serum phospholipid concentrations of fatty acids were generally not related to lower F2-isoprostane levels. No overall effect from whole grains or fruits and vegetables was seen. ConclusionsThe results indicate that high intake of fatty fish is related to lower levels of oxidative stress, but high levels of ω-3 fatty acids in intake may not alone explain the effect. High habitual intake of whole grains or fruits and vegetables did not seem to affect the F2-isoprostane level.

Fish oil and multivitamin supplementation reduces oxidative stress but not inflammation in healthy older adults: A randomised controlled trial

The effects of daily fish oil supplementation, with and without multivitamins, on biochemical markers of health were examined. Healthy adults (N = 160) were randomised to receive 3 g of salmon oil with a multivitamin, 6 g of salmon oil with a multivitamin, 6 g of salmon oil in isolation or placebo in a double-blind fashion on a daily basis for 16 weeks. Relative to placebo, both 6 g salmon oil groups displayed significantly lower F2-isoprostane levels at endpoint. Increases in red blood cell polyunsaturated fatty acids correlated with reductions in F2-isoprostanes. Treatment had no effect on inflammatory cytokines, C-reactive protein, fibrinogen, cholesterol or triacylglycerol.

37 - Levels of F2-Isoprostanes in Cerebrospinal Fluid after Traumatic Brain Injury Correlated with Poor Outcome of the Patients

37 - Levels of F2-Isoprostanes in Cerebrospinal Fluid after Traumatic Brain Injury Correlated with Poor Outcome of the Patients

Passive smoking reduces and vitamin C increases exercise-induced oxidative stress: Does this make passive smoking an anti-oxidant and vitamin C a pro-oxidant stimulus?

The current interpretative framework states that, for a certain experimental treatment (usually a chemical substance) to be classified as “anti-oxidant”, it must possess the property of reducing (or even nullifying) exercise-induced oxidative stress. The aim of the study was to compare side by side, in the same experimental setup, redox biomarkers responses to an identical acute eccentric exercise session, before and after chronic passive smoking (considered a pro-oxidant stimulus) or vitamin C supplementation (considered an anti-oxidant stimulus). Twenty men were randomly assigned into either passive smoking or vitamin C group. All participants performed two acute eccentric exercise sessions, one before and one after either exposure to passive smoking or vitamin C supplementation for 12days. Vitamin C, oxidant biomarkers (F2-isoprostanes and protein carbonyls) and the non-enzymatic antioxidant (glutathione) were measured, before and after passive smoking, vitamin C supplementation or exercise. It was found that chronic exposure to passive smoking increased the level of F2-isoprostanes and decreased the level of glutathione at rest, resulting in minimal increase or absence of oxidative stress after exercise. Conversely, chronic supplementation with vitamin C decreased the level of F2-isoprostanes and increased the level of glutathione at rest, resulting in marked exercise-induced oxidative stress. Contrary to the current scientific consensus, our results show that, when a pro-oxidant stimulus is chronically delivered, it is more likely that oxidative stress induced by subsequent exercise is decreased and not increased. Reversely, it is more likely to find greater exercise-induced oxidative stress after previous exposure to an anti-oxidant stimulus. We believe that the proposed framework will be a useful tool to reach more pragmatic explanations of redox biology phenomena.