The aim of this study was to determine the influence of long-term docosahexaenoic acid (DHA) dietary supplementation on the erythrocyte fatty acid profile and oxidative balance in soccer players after training and acute exercise. Fifteen volunteer male athletes (age 20.0± 0.5 years) were randomly assigned to a placebo group that consumed an almond-based beverage (n = 6), or to an experimental group that consumed the same beverage enriched with DHA (n = 9) for 8 weeks. Blood samples were taken in resting conditions at the beginning and after 8 weeks of nutritionalintervention and training in resting and in post-exercise conditions. Oxidative damage markers (malonyldialdehyde, carbonyl and nitrotyrosine indexes) and the activity and protein level of antioxidant enzymes (catalase, superoxide dismutase, glutathione reductase and peroxidase) were assessed. The results showed that training increased antioxidant enzyme activities in erythrocytes. The experimental beverage increased DHA from 34.0 ± 3.6 to 43.0 ± 3.6 nmol/10(9) erythrocytes. DHA supplementation increased the catalytic activity of superoxide dismutase from 1.48 ± 0.40 to 10.5 ± 0.35 pkat/10(9) erythrocytes, and brought about a reduction in peroxidative damage induced by training or exercise. In conclusion, dietary supplementation with DHA changed the erythrocyte membrane composition, provided antioxidant defense and reduced protein peroxidative damage in the red blood cells of professional athletes after an 8-week training season and acute exercise.

OBJECTIVE To assess the effect of yoga on anthropometry, blood pressure, glycemic control, and oxidative stress in type 2 diabetic patients on standard care in comparison with standard care alone. RESEARCH DESIGN AND METHODS The study involved 123 patients stratified according to groups with microvascular complications, macrovascular complications, and peripheral neuropathy and without complications and assigned to receive either standard care or standard care along with additional yoga for 3 months. RESULTS In comparison with standard care alone, yoga resulted in significant reduction in BMI, glycemic control, and malondialdehyde and increase in glutathione and vitamin C. There were no differences in waist circumference, waist-to-hip ratio, blood pressure, vitamin E, or superoxide dismutase in the yoga group at follow-up. CONCLUSIONS Yoga can be used as an effective therapy in reducing oxidative stress in type 2 diabetes. Yoga in addition to standard care helps reduce BMI and improve glycemic control in type 2 diabetic patients.

Epidemiological studies indicate that patients with type 2 diabetes mellitus (T2DM) are at increased risk of developing dementia/Alzheimer's disease (AD). This review, which is based on recent studies, presents a molecular framework that links the two diseases and explains how physical training could help counteract neurodegeneration in T2DM patients. Inflammatory, oxidative, and metabolic changes in T2DM patients cause cerebrovascular complications and can lead to blood-brain-barrier (BBB) breakdown. Peripherally increased pro-inflammatory molecules can then pass the BBB more easily and activate stress-activated pathways, thereby promoting key pathological features of dementia/AD such as brain insulin resistance, mitochondrial dysfunction, and accumulation of neurotoxic beta-amyloid (Aβ) oligomers, leading to synaptic loss, neuronal dysfunction, and cell death. Ceramides can also pass the BBB, induce pro-inflammatory reactions, and disturb brain insulin signaling. In a vicious circle, oxidative stress and the pro-inflammatory environment intensify, leading to further cognitive decline. Low testosterone levels might be a common risk factor in T2DM and AD. Regular physical exercise reinforces antioxidative capacity, reduces oxidative stress, and has anti-inflammatory effects. It improves endothelial function and might increase brain capillarization. Physical training can further counteract dyslipidemia and reduce increased ceramide levels. It might also improve Aβ clearance by up-regulating Aβ transporters and, in some cases, increase basal testosterone levels. In addition, regular physical activity can induce neurogenesis. Physical training should therefore be emphasized as a part of prevention programs developed for diabetic patients to minimize the risk of the onset of neurodegenerative diseases among this specific patient group.

Pancreaticβ-cell death or dysfunction mediated by oxidative stress underlies the development and progression of diabetes mellitus (DM). In this study, we evaluated the effect of lentinan (LNT), an active ingredient purified from the bodies of Lentinus edodes, on pancreatic β-cell apoptosis and dysfunction caused by streptozotocin (STZ) and the possible mechanisms implicated. The rat insulinoma cell line INS-1 were pre-treated with the indicated concentration of LNT for 30 min. and then incubated for 24 hrs with or without 0.5 mM STZ. We found that STZ treatment causes apoptosis of INS-1 cells by enhancement of intracellular reactive oxygen species (ROS) accumulation, inducible nitric oxide synthase (iNOS) expression and nitric oxide release and activation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signalling pathways. However, LNT significantly increasedcell viability and effectively attenuated STZ-induced ROS production, iNOS expression and nitric oxide release and the activation of JNK and p38 MAPK in a dose-dependent manner in vitro. Moreover, LNT dose-dependently prevented STZ-induced inhibition of insulin synthesis by blocking the activationof nuclear factor kappa beta and increasing the level of Pdx-1 in INS-1 cells. Together these findings suggest that LNT could protect against pancreatic β-cell apoptosis and dysfunction caused by STZ and therefore may be a potential pharmacological agent for preventing pancreatic β-cell damage caused by oxidative stress associated with diabetes.

Background Oxidative stress plays a critical role in the pathogenesis and progression of type 2 diabetes and diabetic-associated cardiovascular complications. This study investigated the impact of crocin combined with voluntary exercise on heart oxidative stress indicator in high-fat diet-induced type 2 diabetic rats.

Materials and methods Rats were divided into four groups: diabetes, diabetic-crocin, diabetic-voluntary exercise, diabetic-crocin-voluntary exercise. Type 2 diabetes was induced by high-fat diet (4 weeks) and injection of streptozotocin (intraperitoneally, 35 mg/kg). Animals received crocin orally (50 mg/kg); voluntary exercise was performed alone or combined with crocin treatment for 8 weeks. Finally, malondialdehyde (MDA), activity of antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were measured spectrophotometrically.

Results Treatment of diabetic rats with crocin and exercise significantly decreased the levels of MDA (p < 0.001) and increased the activity of SOD, GPx, and CAT compared with the untreated diabetic group. In addition, combination of exercise and crocin amplified their effect on antioxidant levels in the heart tissue of type 2 diabetic rats.

Conclusion We suggest that a combination of crocin with voluntary exercise treatment may cause more beneficial effects in antioxidant defense system of heart tissues than the use of crocin or voluntary exercise alone.

BACKGROUND:The metabolic syndrome leads to high morbidity and mortality. Almost all pathological states are associated with oxidative stress (OS) disorders. This study evaluates the effects of Coenzyme Q10 (CoQ10) supplementation on different lifestyles, in relation to serum and tissue OS parameters.

MATERIALS AND METHODS:Twelve Wistar rat groups (10 rats/group) were equally divided in three types of diets: standard (St), high fat (HF), high sugar (HS); within each diet group there was one sedentary group with CoQ10 supplementation (100 mg/kg body weight), one sedentary without CoQ10, one trained group with CoQ10 and one trained group without CoQ10 supplementation. After 28 days blood samples were collected as follows: after 12 hours of fasting (T0), 1 hour postprandial (T1) and after 1 hour of exercise (T2) or sedentary postprandial time (T3). Thiol groups (SH) and malondialdehyde (MDA) were determined from serum and liver homogenate.

RESULTS:Significant changes were observed in fasting MDA for HF (p = 0.024 for training, 0.028 for CoQ10). Postprandial, OS status altered, with highest MDA in HF sedentary non-CoQ10 group (3.92 ± 0.37 vs 2.67 ± 0.41 nmol/ml in St trained CoQ10). At T2 the untrained and non-CoQ10 groups had the highest MDA levels (up to 22.3% vs T1, p < 0.001 in HF) as SH dropped (34.4% decrease vs T1, p < 0.001 in HF). At T3 high MDA levels were observed, correlated with low SH (Pearson r = -0.423 overall), irrespective of the CoQ10 supplementation. CoQ10 improved the liver OS status (MDA and SH decreased), but not the exercise, in all diets.

CONCLUSIONS:CoQ10 supplementation accompanied by chronic exercise improved the OS serum profile, irrespective of the daily diet. CoQ10 lowered liver MDA and SH concentrations.

Studies about Coenzyme Q10 (CoQ10 ) supplementation on strenuous exercise are scarce, especially those related with oxidative stress associated with physical activity and virtually nonexistent with the reduced form, Ubiquinol. The objective of this study was to determine, for the first time, whether a short-term supplementation with Ubiquinol can prevent oxidative stress associated to strenuous exercise. The participants (n = 100 healthy and well trained, but not on an elite level) were classified in two groups: Ubiquinol (experimental group), and placebo group (control). The protocol consisted of conducting two identical strenuous exercise tests with a rest period between tests of 24 h. Blood and urine samples were collected from the participants before supplementation (basal value) (T1), after supplementation (2 weeks) (T2), after first physical exercise test (T3), after 24 h of rest (T4), and after second physical exercise test (T5).The increase observed in the lactate, isoprostanes, DNA damage, and hydroperoxide levels reveals the severity of the oxidative damage induced by the exercise. There was a reduction in the isoprostanes, 8-OHdG, oxidized LDL, and hydroperoxydes in the supplemented Ubiquinol group, an increase in total antioxidant status, fat soluble antioxidant (both plasma and membrane),and CAT activity. Also, NO in the Ubiquinol-supplemented group was maintained within a narrow range. Oxidative stress induced by strenuous exercise is accumulative and increases transiently in subsequent sessions of physical activity. A short-term supplementation (2 weeks) with Ubiquinol (200 mg/day) before strenuous exercise, decreases oxidative stress and increases plasma NO, fact that could improve endothelial function, energetic substrate supply, and muscle recovery after strenuous exercise. © 2016 BioFactors, 2016.

The antioxidant effect of pterostilbene on streptozotocin-nicotinamide-induced diabetic rats has been assessed. The activity of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and reduced glutathione was significantly decreased in liver and kidney of diabetic animals when compared with normal control. There were significant improvements in these activities after treatment with pterostilbene at a dose of 40 mg kg(-1) for six weeks. The increased levels of lipid peroxidation measured as thiobarbituric acid reactive substances (TBARS) in liver and kidney of diabetic rats were also normalized by treatment with pterostilbene. Chronic treatment of pterostilbene remarkably reduced the pathological changes observed in liver and kidney of diabetic rats. These results indicated the antioxidant property of pterostilbene.

Diabet. Med. 28, 549-559 (2011) ABSTRACT: Aims  The aim of this study was to compare the effects of calorie-restricted vegetarian and conventional diabetic diets alone and in combination with exercise on insulin resistance, visceral fat and oxidative stress markers in subjects with Type 2 diabetes. Methods  A 24-week, randomized, open, parallel design was used. Seventy-four patients with Type 2 diabetes were randomly assigned to either the experimental group (n = 37), which received a vegetarian diet, or the control group (n = 37), which received a conventional diabetic diet. Both diets were isocaloric, calorie restricted(-500 kcal/day). All meals during the study were provided. The second 12 weeks of the diet were combined with aerobic exercise. Participants were examined at baseline, 12 weeks and 24 weeks. Primary outcomes were: insulin sensitivity measured by hyperinsulinaemic isoglycaemic clamp; volume of visceral and subcutaneous fat measured by magnetic resonance imaging; and oxidative stress measured by thiobarbituric acid reactive substances. Analyses were by intention to treat. Results  Forty-three per cent of participants in the experimental group and 5% of participants in the control groupreduced diabetes medication (P < 0.001). Body weight decreased more in the experimental group than in the control group [-6.2 kg (95% CI -6.6 to -5.3) vs. -3.2 kg (95% CI -3.7 to -2.5); interaction group × time P = 0.001]. An increase in insulin sensitivity was significantly greater in the experimental groupthan in the control group [30% (95% CI 24.5-39) vs. 20% (95% CI 14-25), P = 0.04]. A reduction in both visceral and subcutaneous fat was greater in the experimental group than in the control group (P = 0.007 and P = 0.02, respectively). Plasma adiponectin increased (P = 0.02) and leptin decreased (P = 0.02) in the experimental group, with no change in the control group. Vitamin C, superoxide dismutase and reduced glutathione increased in the experimental group (P = 0.002, P < 0.001 and P = 0.02, respectively). Differences between groups were greater after the addition of exercise training. Changes in insulin sensitivity and enzymatic oxidative stress markers correlated with changes in visceral fat. Conclusions  A calorie-restricted vegetarian diet had greater capacity to improve insulin sensitivity compared with a conventional diabetic diet over 24 weeks. The greater loss of visceral fat and improvements in plasma concentrations of adipokines and oxidative stress markers with this diet may be responsible for the reduction of insulin resistance. The addition of exercise training further augmented the improved outcomes with the vegetarian diet.

The present study evaluated the synergistic effects of the association of ascorbic acid andα-tocopherol on myenteric in the jejunum of diabetic rats. The rats were randomly divided into four equal groups: untreated normoglycemic (UC), untreated diabetic (UD), ascorbic acid and α-tocopherol-treated normoglycemic (CAE) and ascorbic acid and α-tocopherol-treated diabetic (DAE). The rats from the CAE and DAE group received supplementation with ascorbic acid (1g/L in water) and α-tocopherol (1% in chow). At 210-days-old, the animals were sacrified and their jejunum was collected and submitted to immunohistochemistry. Quantitative and/or morphometric analysis were performed. Supplementation with ascorbic acid and α-tocopherol prevented the cell loss of myenteric neurons expressing HuC/D and TrkA in an equivalent proportion. We also observed a reduction of the CGRP nerve fiber varicosities and the prevention of the increased cell body size of submucosal VIP neurons (p<0.05). The association of ascorbic acid andα-tocopherol reduced the deleterious effects of diabetes promoting protection on the enteric neurons.