Oxidative Stress In Healthy Volunteers Research Articles

Efficacy of Vasantik Vaman Karma (Therapeutic Emesis) on Oxidative Stress Markers in Healthy VolunteersA Pilot Randomised Controlled Study

Introduction: Vamana karma is a therapeutic emesis procedure recommended for maintaining health in healthy individuals. It is said to be conducted during the Vasant rutu (spring season) and is referred to as Vasantik Vaman. During this season, there is an aggravation of Kapha dosha, which can lead to various diseases. The bio-purification of the body in Vasant rutu through the Vaman procedure helps to detoxify and rejuvenate the body. To make this practice evidence-based, the present study was planned to evaluate the efficacy of Vamana karma, which is also considered a shodhana karma, in reducing oxidative stress. Aim: To compare the efficacy of Vasantik Vamana karma on Malondialdehyde (MDA) and Superoxide Dismutase (SOD) levels as markers of oxidative stress in healthy volunteers, compared to a non interventional group. Materials and Methods: The present randomised controlled study was conducted in the Department of Kriyasharir, Mahatma Gandhi Ayurved College, Hospital and Research Centre, under the auspices of Datta Meghe Institute of Higher Education University, Wardha, Maharashtra, India, from March 2023 to April 2023 during the Vasant rutu. A total of 58 healthy individuals aged between 20 years and 40 years were sensitised regarding the procedure and benefits of Vasantik Vamana karma. After sensitisation, 30 volunteers who provided written consent for participation in the study were enrolled, examined and randomly divided into two groups: Group A (non interventional) and Group B (interventional). Both groups were assessed on the 0th day and the 15th day for oxidative stress markers, specifically free radicals (MDA) and antioxidant (SOD) levels. Statistical analysis was done using descriptive and inferential statistics, including Student’s paired and unpaired t-tests. Results: The mean±Standard Deviation (SD) age of participants was 21.23±0.37 years, with participation almost equal from both genders. Before the intervention, SOD and MDA levels were similar in both the control and interventional groups. After the intervention of Vasantik Vamana karma, Group B showed an increase in SOD levels and a decrease in MDA levels, which were statistically highly significant according to the paired t-test (p-value≤0.001) in comparison to the non interventional group. In the non interventional group, p-value=0.951 for SOD levels and 0.551 for MDA levels by paired t-test, which were not significant. When both groups were compared using an unpaired test, at pre-intervention, both groups were at the same level, but after the intervention, statistically significant results were observed in Group B (p-value≤0.001). Conclusion: The present study concluded that Vasantik Vamana karma, as a bio-purification process, Vasantik Vamana karma has proven to be highly effective in detoxifying the body by reducing oxidative stress in healthy volunteers.

Effects of Turmeric Concentrate on Cardiovascular Risk Factors and Exercise-Induced Oxidative Stress in Healthy Volunteers; an Exploratory Study.

Evidence suggests that turmeric intake can improve antioxidant defense, blood pressure (BP), ageing and gut microbiota. The effects of turmeric concentrate (curcumin) intake on cardiovascular risk factors and exercise induced oxidative stress were investigated. A randomized placebo-controlled study was performed to assess the effects of turmeric extract in healthy volunteers before and after a 30 min exercise bout. Participants (n=22) were given either turmeric concentrate or placebo supplements. Anthropometry, BP, pulse wave velocity (PWV), biomarkers of oxidative stress, perceived exertion and lipid peroxidation were assessed. In the turmeric group, the expected BP response to exercise following turmeric was blunted and the increase was not significant compared to basal values followed by a decrease in final BP and PWV values. There were no significant differences in all baseline parameters between the placebo and the curcumin groups (P>0.05). A significant increase was observed in urinary antioxidant power (P=0.031) and total polyphenol levels (P=0.022) post turmeric intervention. The distance ran by the participants taking turmeric was significantly longer (P=0.005) compared to basal value. Those who took the placebo did not show significant changes. Our study suggests that turmeric concentrate intake can reduce BP and improve antioxidant, anti-inflammatory status and arterial compliance. Turmeric may improve exercise performance and ameliorates oxidative stress. Larger studies are warranted to validate these findings and test more cardiovascular risk factors.

Regulation of free radical processes in healthy volunteers during experimental hyperthermia and in patients with coronary artery disease during summer heat waves

Background. In view of the worsening forecast for global temperature rise worldwide, it seems relevant to study the effects of abnormal heat waves on systemic regulatory processes in people with chronic diseases, in particular coronary artery disease (CAD).Aims. This study aimed to investigate the effect of hyperthermia on oxidative stress parameters in patients with various severity of CAD and in healthy subjects.Materials and methods. We studied the level of malonic dialdehyde (MDA) and the activity of Cu,Zn-containing superoxide dismutase (Cu,Zn-SOD) in healthy subjects under conditions of 30-day long simulated hyperthermia and in patients with different severity of CAD after the summer heat wavesResults. We revealed signs of oxidative stress in healthy volunteers during model hyperthermia that manifested as an increase in content of MDA in blood plasma. At the same time we observed increasing activity of Cu,Zn-SOD in erythrocytes that utilizes reactive oxygen species. The increase of Cu,Zn-SOD activity started with a certain latency what also can be explained by de novo enzyme biosynthesis induction. We also studied oxidative stress parameters in patients at high and moderate cardiovascular risk according to the SCORE risk chart with uncomplicated CAD course and in patients with complicated CAD with severe coronary damage according to angiography during the summer heat waves. We observed accumulation of MDA in blood plasma and increasing activity of erythrocyte Cu,Zn-SOD in patients with uncomplicated CAD. At the same time we noted that accumulation of MDA in blood plasma was not followed by any increase in activity of red blood cell Cu,Zn-SOD in patients with severe complicated CAD. This fact indicates dysregulation of free radical processes in patients with severe course of CAD during the heat waves.Conclusions. The dysregulation of free-radical processes in patients with a severe clinical course of CAD has been revealed.

Rapid on-site dual optical system to measure specific reactive oxygen species (O2-• and OCl-) in a tiny droplet of whole blood.

Oxidative stress has been implicated in various disorders and controlling it would be important for healthy life. We have developed a new optical system for easily and accurately measuring oxidative stress in whole blood. It is optimized for simultaneously detecting reactive oxygen species (ROS) and highly reactive ROS (hROS), elicited mostly by white blood cells in a few microliters of blood. Results obtained by using this system show at least four important findings. 1) chemiluminescence of MCLA was confirmed to be attributable to O2-•. 2) PMA-stimulated cells released O2-• longer and more slowly than fMLP-stimulated ones. 3) fluorescence produced by APF oxidation was confirmed to be attributable to hROS, mostly OCl-, produced by myeloperoxidase. 4) the generation of OCl- was found to be a slower process than the O2-• generation. We also conducted pilot studies of oxidative stress in healthy volunteers.

A single blueberry (Vaccinium corymbosum) portion does not affect markers of antioxidant defence and oxidative stress in healthy volunteers following cigarette smoking.

We previously reported that a portion of blueberries reversed endothelial dysfunction induced by acute cigarette smoking. Since smoking-induced endothelial dysfunction is associated with a condition of oxidative stress, we evaluated whether the observed effect was mediated by modulation of markers of oxidative stress and antioxidant defence. Fourteen out of 16 male healthy smokers previously enrolled, participated in a three-armed randomized controlled study with the following experimental conditions: smoking treatment (one cigarette); blueberry treatment (300g of blueberries) + smoking (one cigarette); control treatment (300ml of water with sugar) + smoking (one cigarette). The cigarette was smoked 100min after blueberry/control/water consumption. Each treatment was separated by 1 week of washout period. Plasma vitamin (C, B12 and folate) and aminothiol concentrations, endogenous [formamidopyrimidine-DNA glycosylase (FPG)-sensitive sites] and oxidatively induced DNA damage (resistance to H2O2-induced DNA damage) in peripheral blood mononuclear cells (PBMCs) were measured at baseline and 20, 60, 90, 120min and 24h after smoking. On the whole, analysis of variance did not show a significant effect of treatment on the modulation of markers of oxidative stress and antioxidant defence but revealed an effect of time for plasma concentrations of vitamin C (P = 0.003), B12 (P < 0.001), folate (P < 0.001), total cysteine (P = 0.007) and cysteine-glycine (P = 0.010) that increased following the three treatments after smoking. No significant effect of treatment was observed for the levels of FPG-sensitive sites (P > 0.05) and H2O2-induced DNA damage (P > 0.05) in PBMCs. In conclusion, the consumption of a single blueberry portion failed to modulate markers of oxidative stress and antioxidant defence investigated in our experimental conditions. Further studies are necessary to elucidate this finding and help clarifying the mechanisms of protection of blueberries against smoking-induced endothelial dysfunction.

Evaluation of antioxidant potential of Rasayana drugs in healthy human volunteers.

Background:It is increasingly being realized that many of today's diseases are due to “oxidative stress” that results from an imbalance between formation and neutralization of free radicals. Rasayana Chikitsa is a unique branch of Ayurveda. The word Rasayana means the way for attaining excellent Rasadi Dhatus. Several medicinal plants have been described as Rasayanas in Ayurveda. Ashwagandha and Guduchi are the best among the Rasayanas described by Charaka.Aim:To study the efficacy of Ashwagandha and Guduchi in oxidative stress in healthy volunteers.Materials and Methods:The study was carried out on 30 healthy volunteers after obtaining written informed consent. They were randomly distributed in three groups. Each group was treated with three different colored capsules containing Ashwagandha, Guduchi and placebo in the dose of 1 capsule (500 mg) twice a day for 6 months. The parameters such as hemoglobin%, Erythorcyte Sedimentation Rate (ESR), Malondialdehyde (MDA), Super-Oxide Dismutase (SOD) level, etc., were assessed before and after treatment. The Student's t-test was applied to assess significant variations in all of the studied parameters.Results:In this study, there was a significant increase in SOD level and decrease in MDA level in Ashwagandha and Guduchi groups.Conclusion:Ashwagandha and Guduchi may be helpful in preventing the oxidative stress and premature aging.

Impact of Ramadan Intermittent Fasting on Oxidative Stress Measured by Urinary 15-F2t-Isoprostane

Fasting and caloric restriction have been associated with reduced incidence of chronic diseases and cancers. These effects have been attributed to reduced oxidative stress. Since Ramadan intermittent fasting (RIF) has been associated with reduced caloric intake, it was hypothesized that RIF would alleviate oxidative stress in healthy volunteers. The study was designed to elucidate the impact of RIF on oxidative stress measured by 15-F2t-Isoprostane (15FIP). Fifty healthy subjects (23 men and 27 women) who intended to fast Ramadan were recruited. Urine and serum sampling and anthropometric and dietary assessments were conducted one week before Ramadan (T0), at the end of the third week of Ramadan (T1), and one month after Ramadan (T2). Biochemical measurements included urinary 15FIP, creatinine, and hematological indices. Results revealed that the urinary level of 15FIP measured at T0 was normal, while they showed a significantly (P < 0.05) higher level when measured at T1 concomitant with a significant (P < 0.05) increase in the body weight and total body fat percent. In conclusion, results suggest that increased body weight is associated with increased lipid peroxidation and oxidative stress, and the impact of RIF on oxidative stress is mediated by the changes in body weight at the end of the month.

Effects of acetylsalicylic acid on serum paraoxonase activity, Ox-LDL, coenzyme Q 10 and other oxidative stress markers in healthy volunteers

Objectives: The aim of the study was to examine the effects of acetylsalicylic acid (ASA) on oxidative stress in healthy volunteers. Design and Methods: 30 volunteers of which 17 received ASA as 100 mg/day (Group I) and 13 received ASA as 150 mg/day (Group II) for 2 months. Serum paraoxonase 1 (PON1), arylesterase, total antioxidant status (TAS), total oxidant status (TOS), oxidized LDL (Ox-LDL) and coenzyme Q 10 (CoQ 10) levels were measured before and 1 and 2 months after treatment. Results: There was no significant differences between the measured parameters of the groups. However, TOS and Ox-LDL levels of group II were significantly reduced after 2 months of treatment ( p < 0.05). Conclusions: Significantly inhibition of LDL oxidation and significantly reduction in TOS levels of group II after 2 months of ASA treatment shows that ASA treatment may contribute to the prevention of atherosclerosis, a beneficial effect which is dose and time dependent.

A Single High Dose of Ascorbic Acid and Iron Is Not Correlated with Oxidative Stress in Healthy Volunteers

Fe (II) is a potential prooxidant in vivo and can induce cellular oxidative stress. Ascorbic acid (AA) is a powerful physiological antioxidant and, in the presence of free Fe (II), can exhibit prooxidant effects in vitro. However, in vivo prooxidant effects of Fe (II) and AA have not yet been indisputably demonstrated. Here we evaluate the potential toxic effect of supplementation of Fe (II) associated with AA. Nine healthy, nonsmoking male volunteers (20–31 years old) participated in the crossover study design. The volunteers were supplemented with either a dose of 2 g of AA, 150 mg of iron carbonyl or 2 g of AA plus 150 mg of iron carbonyl with a washout period of 15 days between each treatment. AA, iron, ferritin, thiobarbituric acid-reactive substances, catalase, δ-aminolevulinic dehydratase and SH thiol groups were measured in the blood of the volunteers. Plasma AA levels were increased at 2, 5 and 24 h after AA or AA plus iron ingestion. Plasma Fe levels were increased at 2 and 5 h in the AA plus iron group. Erythrocyte malondialdehyde levels decreased at 5 and 24 h after AA and 5 h after AA plus iron ingestion. Catalase activity from erythrocytes was increased 5 h after supplementation with AA plus iron. There was no significant difference between groups in the other biochemical parameters evaluated. Thus, the present study does not support the hypothesis that the combination of high plasma concentrations of AA and iron, or iron alone, could cause in vivo oxidative damage after a single supplementation dose.

Effect of 4 days of intermittent hypoxia on oxidative stress in healthy men

Periodic occlusion of the upper airway in patients with obstructive sleep apnea (OSA) leads to intermittent hypoxia (IH). IH is characterized by repeated episodes of hypoxia/reoxygenation, which is known to increase the production of reactive oxygen species (ROS). Causal relationships between OSA, IH and oxidative stress have not been established because of confounding effects of medical co‐morbidities and obesity which are frequently associated with OSA. The aim of this study was to determine if IH changes oxidative stress in healthy volunteers. Nine men (29.3 ± 1.7 years; BMI, 25.0 ± 0.4 kg.m−2; mean±SD) were studied. Following baseline measurements breathing room air (day zero (D0)), all subjects were exposed to 4 days (D1 to D4) of IH while awake (2 min at PetO2 = 45 Torr and 2 min at PetO2 = 88 Torr) 6 hours.d−1. Lipid peroxidation (malondialdehides, MDA), DNA oxidation (8‐Hydroxy‐2′‐deoxyguanosine, 8‐OHdG) and oxidation protein products (AOPP) were assessed in plasma. MDA increased significantly between baseline (D0) and D1 (+39%: 3.48 ± 1.17 vs 4.85 ± 0.90 μmol.l−1) and then tended to return to baseline levels. 8‐OHdG increased significantly between D0 and D1 (+51%: 53.84 ± 54.63 vs 83.30 ± 45.49 μmol.l−1) and remained elevated until D4 (+67%: 53.84 ± 54.63 vs 89.71 ± 36.06 μmol.l−1). These findings demonstrate that IH increases oxidative stress and suggest that IH may contribute to ROS overproduction in OSA.Supported by the Alberta Heritage Foundation for Medical Research and the Heart &amp; Stroke Foundation of Canada.

Effect of hyperbaric oxygen and vitamin C and E supplementation on biomarkers of oxidative stress in healthy men

The objectives of the present study were to evaluate the effect of normobaric and hyperbaric O2 (HBO) on plasma antioxidants and biomarkers of oxidative stress in plasma and urine and to investigate the effect of a 4-week vitamin C plus E supplementation on HBO-induced oxidative stress. Nineteen healthy men were exposed to HBO (100 % O2; 240 kPa) before and after 4 weeks' supplementation with 500 mg vitamin C plus 165 mg alpha-tocopherol equivalents. Exposure to 21 % O2 at 100 kPa served as intra-individual controls (control). Samples for the analysis of plasma antioxidants and oxidative stress biomarkers were collected before and immediately after each treatment. The present results showed that when compared with 'control', a single exposure to HBO resulted in a decrease of plasma vitamin C (P = 0.027) and an increase of lipid peroxides (P = 0.0008) and urinary 8-oxo-deoxyguanosine (8-oxodG) excretion (P = 0.006). Oxidative stress was not prevented by a 4-week supplementation with vitamins C and E. HBO-induced changes in plasma parameters correlated with basal antioxidant levels. The increase of urinary 8-oxodG after HBO plus supplementation correlated negatively with vitamin E intake (P = 0.023). We concluded that in healthy men HBO caused oxidative stress, which could not be prevented by dietary vitamin C plus E supplementation. The present data support the idea that HBO is a suitable model for oxidative stress in healthy volunteers.

Effects of vitamin E depletion/repletion on vitamin E status and oxidative stress in healthy volunteers

Effects of vitamin E depletion/repletion on vitamin E status and oxidative stress in healthy volunteers

Effects of a high-fat meal on resistance vessel reactivity and on indicators of oxidative stress in healthy volunteers.

High fat meals postprandially impair macrovascular endothelial function and a link to increased oxidative stress is suggested. Few information, on the other hand, exists on the effect of postprandial hyperlipidaemia on resistance vessel function. Under normal circumstances this vascular bed regulates tissue perfusion and, by controlling flow, impacts on macrovascular nitric oxide formation. The impact of a high fat meal (1200 kcal, 90 g fat, 46 g protein and 47 g carbohydrates) on postprandial resistance vessel reactivity and on indicators of oxidative stress was studied in 11 healthy subjects by venous-occlusion plethysmography using another six subjects as time control group. Ingestion of the test meal resulted in a pronounced increase of serum triglycerides from 1.05 +/- 0.61 mmol l(-1) in the fasting state to peak postprandial values of 1.94 +/- 0.41 mmol l(-1) (P < 0.001) reached after 4 h and a return to baseline after 8 h. Fasting peak reactive hyperaemia (RH) was 19.6 +/- 2.4 ml min(-1) (100 ml)(-1). Two hours after ingestion of the test meal peak RH was transiently reduced to 16.8 +/- 2.2 ml min(-1) (100 ml)(-1) (P < 0.05). No alteration of resting forearm perfusion was observed. The time course of peak RH suggested a potential biphasic effect of the test meal with an early impairment and a late increase of RH. Ingestion of a lipid rich test meal did not exert any influence on either total plasma antioxidant capacity given in trolox equivalents (513 +/- 26 micromol l(-1) at baseline) or on plasma peroxides measured as H2O2 equivalents (469 +/- 117 micromol l(-1)). Our results suggest that ingestion of a meal containing 90 g of fat results in a transient impairment of reactive hyperaemia in healthy subjects but these vascular alterations are not accompanied by signs of systemically increased oxidative stress.

A multi-biomarker approach to study the effects of smoking on oxidative DNA damage and repair and antioxidative defense mechanisms.

We investigated the effects of smoking-induced oxidative stress in healthy volunteers (21 smokers versus 24 non-smokers) by quantifying various markers of oxidative DNA damage and repair, and antioxidative defense mechanisms. Lymphocytic 7-hydroxy-8-oxo-2'-deoxyguanosine (8-oxo-dG) levels measured by high performance liquid chromatography with electrochemical detection, were significantly lower in smokers as compared with non-smokers (38.6 +/- 5.2 versus 50.9 +/- 4.6/10(6) dG, P = 0.05). The levels of oxidized pyrimidine bases in lymphocytes of smokers quantified by the endonuclease III-modified comet assay were non-significantly lower than those of non-smokers (% DNA in tail: 13 +/- 3 versus 14 +/- 2; tail length: 69 +/- 13 versus 96 +/- 10; tail moment: 6416 +/- 1220 versus 7545 +/- 1234). Urinary excretion levels of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) assessed by enzyme-linked immunosorbent assay did not differ significantly between smokers and non-smokers (197 +/- 31 versus 240 +/- 33 ng/body mass index, P = 0.3). Overall DNA repair activity expressed as unscheduled DNA synthesis in blood leukocytes, was not significantly different between smokers and non-smokers (2.9 +/- 0.3 versus 3.3 +/- 0.3, P = 0.4). Plasma antioxidative capacity measured by the Trolox equivalent antioxidant capacity assay was slightly higher in smokers as compared with non-smokers (440 +/- 16 versus 400 +/- 15 microM Trolox equivalent, P = 0.09), and it was significantly related to lymphocytic 8-oxo-dG levels (r = 0.4, P = 0.001). Genotyping of human 8-OH-dG glycosylase/apurinic lyase and glutathione S-transferase M1 showed that a polymorphism in either or both of the two genes does not affect any of the quantified biomarkers. We conclude that oxidative stress imposed by cigarette smoking has a low impact upon certain pathways involved in DNA damage and the antioxidative defense system.

Does free fatty acid infusion impair insulin action also through an increase in oxidative stress?

In vitro studies have demonstrated that free fatty acids (FFA) may enhance oxidative stress. In contrast, no in vivo studies have addressed such a relationship. This four-part study aims at investigating the association between FFA and oxidative stress in healthy volunteers. The following experimental procedures were carried out: 1) determination and simple correlations among fasting plasma FFA, glucose, insulin, plasma thiobarbituric acid-reactive substance (TBARS), the ratio of reduced glutathione (GSH) to oxidized GSH, and lipid hydroperoxide (n = 30); 2) time-dependent effect of FFA on plasma TBARS concentrations and GSH/oxidized GSH ratio (n = 10); 3) dose-dependent effect of FFA on plasma TBARS concentrations (n = 9); and 4) relationship among plasma FFA concentrations, plasma TBARS concentrations, and insulin action (n = 11). The results demonstrate that fasting plasma FFA concentrations correlated with fasting plasma TBARS concentrations (r = 0.65; P < 0.001) and lipid hydroperoxide (r = 0.79; P < 0.001). The correlation between plasma FFA and TBARS remained significant even after adjustment for age, sex, body mass index, and fasting and 2-h plasma glucose concentrations (r = 0.43; P < 0.01). In the time-dependent study, plasma TBARS concentrations increased with the rise in plasma FFA concentrations. In the dose-response study, a progressive increase in fasting plasma FFA concentrations was achieved by varying the Intralipid infusion rate, which also caused plasma TBARS concentrations to increase progressively until they reached a plateau between the last two infusion rates (0.3 and 0.4 mL/min). A euglycemic hyperinsulinemic glucose clamp (insulin infusion rate, 10.2 pmol/kg min for 360 min) was also performed. Simultaneous 10% Intralipid (0.4 mL/min) infusion significantly enhanced plasma TBARS concentrations and inhibited insulin-stimulated whole body glucose disposal (WBGD). GSH infusion (15 mg/min for 360 min) had opposite effects on plasma TBARS concentrations and WBGD. A combined infusion of 10% Intralipid and GSH was associated with a stimulation of WBGD with a magnitude midway between that of 10% Intralipid and GSH infused separately. In conclusion, fasting plasma FFA seems to enhances oxidative stress, which might contribute to the disruptive effects of plasma FFA on insulin-mediated glucose uptake.

Does free fatty acid infusion impair insulin action also through an increase in oxidative stress?

In vitro studies have demonstrated that free fatty acids (FFA) may enhance oxidative stress. In contrast, no in vivo studies have addressed such a relationship. This four-part study aims at investigating the association between FFA and oxidative stress in healthy volunteers. The following experimental procedures were carried out: 1) determination and simple correlations among fasting plasma FFA, glucose, insulin, plasma thiobarbituric acid-reactive substance (TBARS), the ratio of reduced glutathione (GSH) to oxidized GSH, and lipid hydroperoxide (n = 30); 2) time-dependent effect of FFA on plasma TBARS concentrations and GSH/oxidized GSH ratio (n = 10); 3) dose-dependent effect of FFA on plasma TBARS concentrations (n = 9); and 4) relationship among plasma FFA concentrations, plasma TBARS concentrations, and insulin action (n = 11). The results demonstrate that fasting plasma FFA concentrations correlated with fasting plasma TBARS concentrations (r = 0.65; P < 0.001) and lipid hydroperoxide (r = 0.79; P < 0.001). The correlation between plasma FFA and TBARS remained significant even after adjustment for age, sex, body mass index, and fasting and 2-h plasma glucose concentrations (r = 0.43; P < 0.01). In the time-dependent study, plasma TBARS concentrations increased with the rise in plasma FFA concentrations. In the dose-response study, a progressive increase in fasting plasma FFA concentrations was achieved by varying the Intralipid infusion rate, which also caused plasma TBARS concentrations to increase progressively until they reached a plateau between the last two infusion rates (0.3 and 0.4 mL/min). A euglycemic hyperinsulinemic glucose clamp (insulin infusion rate, 10.2 pmol/kg min for 360 min) was also performed. Simultaneous 10% Intralipid (0.4 mL/min) infusion significantly enhanced plasma TBARS concentrations and inhibited insulin-stimulated whole body glucose disposal (WBGD). GSH infusion (15 mg/min for 360 min) had opposite effects on plasma TBARS concentrations and WBGD. A combined infusion of 10% Intralipid and GSH was associated with a stimulation of WBGD with a magnitude midway between that of 10% Intralipid and GSH infused separately. In conclusion, fasting plasma FFA seems to enhances oxidative stress, which might contribute to the disruptive effects of plasma FFA on insulin-mediated glucose uptake.