Plasma Thiobarbituric Acid Reactive Substances Research Articles

Influence of specific endothelin-1 receptor blockers on hemodynamic parameters and antioxidant status of plasma in LPS-induced endotoxemia

BackgroundThe potent vasoconstrictor endothelin-1 has been implicated in the pathogenesis of plasma oxidative stress seen in sepsis. The selective endothelin receptor blockers BQ123 andBQ788 were used to investigate the importance of selective endothelin receptor blockage in modulating oxidative stress during endotoxemia. MethodsThe study was performed on male Wistar rats (n=6 per group) divided into groups: (1) saline, (2) lipopolysaccharide (LPS) (15mg\\kg)-saline, (3) BQ123 (0.5mg\\kg)-LPS, (4) BQ123 (1mg\\kg)-LPS, (5) BQ788 (3mg\\kg)-LPS. The endothelin receptor type A (ETA-R) or type B (ETB-R) antagonist was injected intravenously 30min before LPS administration. Blood pressure was monitored and blood was taken before, 90min and 300min after saline or LPS administration. ResultsInjection of LPS alone resulted in a decrease in mean arterial pressure (MAP) (p<0.05), a decrease in ferric reducing ability of plasma (FRAP) value (p<0.01) and a marked increase in plasma tumor necrosis factor α (TNF-α) and thiobarbituric acid reactive substances (TBARS) (p<0.001, p<0.001, respectively). Administration of BQ123 before LPS administration deteriorated MAP in a dose dependent way. Moreover, BQ123 (1mg\\kg) decreased plasma level of TBARS and TNF-α (p<0.01 and p<0.05, respectively) and increased FRAP value (p<0.001). On the contrary, BQ788 prevented LPS-induced decrease in MAP (p<0.001) and led to a significant reduction in plasma TBARS concentration (p<0.01). ConclusionOur study showed that blockage of ETB-R during endotoxemia improved blood hemodynamics and decreased plasma lipid peroxidation. Blockage of ETA-R improved plasma antioxidant status and decreased lipid peroxidation and TNF-a production, but it deteriorated hemodynamic conditions.

Oxidative stress is associated with visceral adipose tissue and subclinical atherosclerosis in a healthy multi-ethnic population

Oxidative stress plays an important role in the development of atherosclerosis. Excess visceral adipose tissue (VAT) and increased carotid intima-media thickness (IMT) are risk factors for coronary artery disease. We tested the hypothesis that VAT and IMT were associated with systemic oxidative stress. Healthy men and women (n = 565) matched for ethnicity (Aboriginal, Chinese, European, and South Asian) were recruited. Plasma malondialdehyde, a biomarker of oxidative stress, was measured as thiobarbituric acid reactive substances (TBARS). VAT and IMT were determined by computerized tomography and ultrasound scans, respectively. Plasma TBARS levels correlated with VAT and total atheroma burden (sum of IMT area and plaque area) in the entire cohort. When stratified by ethnicity, plasma TBARS levels correlated with distinct body composition and arterial measures in different ethnic populations with more associations present amongst Chinese and Europeans relative to Aboriginals and South Asians. VAT was associated with plasma TBARS levels independent of age, sex, ethnicity, smoking, and body mass index. Plasma TBARS levels were associated with IMT, the presence of plaques, and total atheroma burden, independent of age, sex, ethnicity, smoking, body mass index, and VAT. The association with total atheroma burden remained significant even when adjusted for apolipoprotein B. Results from the present study indicate that oxidative stress is positively associated with VAT as well as diffuse and focal carotid atherosclerosis in apparently healthy men and women.

Acute ethanol intake induces superoxide anion generation and mitogen-activated protein kinase phosphorylation in rat aorta: A role for angiotensin type 1 receptor

Ethanol intake is associated with increase in blood pressure, through unknown mechanisms. We hypothesized that acute ethanol intake enhances vascular oxidative stress and induces vascular dysfunction through renin–angiotensin system (RAS) activation. Ethanol (1g/kg; p.o. gavage) effects were assessed within 30min in male Wistar rats. The transient decrease in blood pressure induced by ethanol was not affected by the previous administration of losartan (10mg/kg; p.o. gavage), a selective AT1 receptor antagonist. Acute ethanol intake increased plasma renin activity (PRA), angiotensin converting enzyme (ACE) activity, plasma angiotensin I (ANG I) and angiotensin II (ANG II) levels. Ethanol induced systemic and vascular oxidative stress, evidenced by increased plasma thiobarbituric acid-reacting substances (TBARS) levels, NAD(P)H oxidase‐mediated vascular generation of superoxide anion and p47phox translocation (cytosol to membrane). These effects were prevented by losartan. Isolated aortas from ethanol-treated rats displayed increased p38MAPK and SAPK/JNK phosphorylation. Losartan inhibited ethanol-induced increase in the phosphorylation of these kinases. Ethanol intake decreased acetylcholine-induced relaxation and increased phenylephrine-induced contraction in endothelium-intact aortas. Ethanol significantly decreased plasma and aortic nitrate levels. These changes in vascular reactivity and in the end product of endogenous nitric oxide metabolism were not affected by losartan. Our study provides novel evidence that acute ethanol intake stimulates RAS activity and induces vascular oxidative stress and redox-signaling activation through AT1-dependent mechanisms. These findings highlight the importance of RAS in acute ethanol-induced oxidative damage.

Hyperglycemia-induced oxidative stress is independent of excess abdominal adiposity in normal-weight women with polycystic ovary syndrome

What is the effect of glucose ingestion on leukocytic reactive oxygen species (ROS) generation in normal-weight women with polycystic ovary syndrome (PCOS) with and without excess abdominal adiposity (AA)? Normal-weight women with PCOS exhibit an increase in leukocytic ROS generation in response to glucose ingestion, and this increase is independent of excess AA. Excess adipose tissue is a source of oxidative stress. Normal-weight women with PCOS exhibit oxidative stress and can have excess AA. This is a cross-sectional study involving 30 reproductive-age women. Fourteen normal-weight women with PCOS (6 normal AA, 8 excess AA) and 16 body composition-matched controls (8 normal AA, 8 excess AA) underwent body composition assessment by dual-energy absorptiometry and an oral glucose tolerance test (OGTT) at a university medical center. Insulin sensitivity was derived from the OGTT (IS(OGTT)). Blood was drawn while fasting and 2 h after glucose ingestion to measure leukocytic ROS generation and p47(phox) protein content and plasma thiobarbituric acid-reactive substances (TBARS) and C-reactive protein (CRP). Compared with controls, both PCOS groups exhibited lower IS(OGTT) (43-54%) and greater percentage change (% change) in ROS generation (96-140%), p47(phox) protein (18-28%) and TBARS (17-48%). Compared with women with PCOS with excess AA, those with normal AA exhibited higher testosterone levels (29%) and lower CRP levels (70%). For the combined groups, IS(OGTT) was negatively correlated with the % change in ROS generation and p47(phox) protein. CRP was positively correlated with abdominal fat. The % change in p47(phox) protein was positively correlated with CRP and androgens. Although this study is adequately powered to assess differences in ROS generation between the women with PCOS and control participants, the modest sample size merits caution when interpreting the corroborative results of the additional measures of oxidative stress and inflammation. This study highlights the unique pro-oxidant contribution of circulating leukocytes in the development of insulin resistance and hyperandrogenism in PCOS. Supported by NIH grant HD-048535 to F.G. The authors have nothing to disclose.

Protective effects of thymol on altered plasma lipid peroxidation and nonenzymic antioxidants in isoproterenol‐induced myocardial infarcted rats

This study evaluates the protective effects of thymol on altered plasma lipid peroxidation products and nonenzymic antioxidants in isoproterenol (ISO)-induced myocardial infarcted rats. Male albino Wistar rats were pre and cotreated with thymol (7.5 mg/kg body weight) daily for 7 days. ISO (100 mg/kg body weight) was subcutaneously injected into rats on 6th and 7th day to induce myocardial infarction (MI). Increased activity/levels of serum creatine kinase-MB (CK-MB), plasma thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes with decreased levels of plasma reduced glutathione (GSH), vitamin C, and vitamin E were observed in ISO-induced myocardial infarcted rats. Pre and cotreatment with thymol (7.5 mg/kg body weight) showed normalized activity of serum CK-MB and near normalized levels of plasma lipid peroxidation products, reduced GSH, vitamin C, and vitamin E in myocardial infarcted rats. Furthermore, the in vitro study on reducing power of thymol confirmed its potent antioxidant action. Thus, thymol protects ISO-induced MI in rats by its antilipid peroxidation and antioxidant properties.

Effects of oxidized corn oil and a synthetic antioxidant blend on performance, oxidative status of tissues, and fresh meat quality in finishing barrows

The objective was to evaluate the effect of feeding oxidized corn oil with or without a dietary antioxidant (AOX) on performance, tissue oxidative status, and meat quality in barrows. One hundred sixty barrows were arranged in a 2 × 2 factorial of treatments in a complete randomized block design with 8 pens per treatment and 5 pigs per pen. Diets contained 5.0 mg/kg of 1 of 2 types of corn oil (fresh or oxidized) with or without antioxidant. Final oxidized oil was produced in a heated container by continuously bubbling air heated to 95°C at a rate of 80 L/min to reach a target peroxide value of approximately 150 and 7.5 mEq/kg in the final diet. After 56 d, barrows fed diets formulated with fresh oil had increased ADG (P = 0.03) and ADFI (P = 0.04) and heavier final BW (P = 0.03) than barrows fed oxidized oil. Increased G:F (P = 0.07) was observed for barrows fed diets with AOX after 28 d of feeding but not after 56 d of feeding (P = 0.67) when compared with barrows not fed AOX. An increase (P = 0.06) in plasma thiobarbituric acid reactive substances (TBARS) values, a decrease (P = 0.03) in plasma glutathione peroxidase (GPx) enzyme activity, and a decrease (P = 0.01) in liver vitamin E concentrations were observed in barrows fed diets with oxidized oil. Dietary AOX reduced plasma protein carbonyl content regardless of oil type (P = 0.04). Barrows fed fresh oil had 4.4% heavier HCW (P = 0.01) and 0.7 percentage units increase in dressing percentage (P = 0.01) compared with barrows fed oxidized oil. Loin TBARS values from barrows fed AOX were lower (P < 0.001) after 14 and 21 d of storage in both fresh and oxidized oil groups. In summary, oxidized oil impaired growth performance and caused oxidation stress. Dietary AOX partially ameliorated the negative effects of oxidized oil in finishing pigs by reducing protein oxidation and improving shelf life.

Effect of a Single Dose of Green Tea Polyphenols on the Blood Markers of Exercise-Induced Oxidative Stress in Soccer Players

To evaluate the effect of acute ingestion of green tea polyphenols (GTP) on blood markers of oxidative stress and muscle damage in soccer players exposed to intense exercise. This randomized, double-blinded study was conducted on 16 players during a general preparation period, when all athletes participated in a strength-training program focused on the development of strength endurance. After ingestion of a single dose of GTP (640 mg) or placebo, all athletes performed an intense muscle-endurance test consisting of 3 sets of 2 strength exercises (bench press, back squat) performed to exhaustion, with a load at 60% 1-repetition maximum and 1-min rests between sets. Blood samples were collected preexercise, 5 min after the muscle-endurance test, and after 24 hr of recovery. Blood plasma was analyzed for the concentrations of thiobarbituric acid-reacting substances (TBARS), uric acid (UA), total catechins, total antioxidant status (TAS), and activity of creatine kinase (CK); at the same time, erythrocytes were assayed for the activity of superoxide dismutase (SOD). In both groups, plasma TBARS, UA, and TAS increased significantly postexercise and remained elevated after a 24-hr recovery period. SOD activity in erythrocytes did not change significantly in response to the muscle-endurance test, whereas in both groups plasma CK activity increased significantly after 24 hr of recovery. Acute intake of GTP cased a slight but significant increase in total plasma catechins. However, GTP was found not to exert a significant effect on measured parameters. Acute ingestion of GTP (640 mg) does not attenuate exercise-induced oxidative stress and muscle damage.

Dietary supplementation with 5-aminolevulinic acid modulates growth performance and inflammatory responses in broiler chickens

The objective of this study was to investigate the effect of dietary supplementation with 5-aminolevulinic acid (5-ALA) on the immune system, inflammatory response, and growth performance of broiler chickens. The levels of cluster of differentiation 3 (CD3) mRNA in the spleens of chickens gradually increased with dietary 5-ALA concentration, while the expression levels of interleukin (IL)-2 decreased. Mitogen-induced proliferation of splenic mononuclear cells and blood mononuclear cell phagocytosis in chickens fed 0.001 and 0.01% 5-ALA-supplemented diets were significantly greater than in chickens fed a basal diet (control). Plasma thiobarbituric acid reactive substance (TBARS) concentration gradually increased along with 5-ALA supplement concentration. These results provide the first evidence that the use of dietary 0.001 and 0.01% 5-ALA supplementation induces the T-cell immune system via mild oxidative stress in chickens. Three hours after Escherichia coli lipopolysaccharide-induced immune stimulation, the levels of mRNA encoding pro-inflammatory cytokines, such as IL-6 and tumor necrosis factor-like ligand 1A (TL1A), in chickens fed a 0.001% 5-ALA-supplemented diet were significantly lower than those in chickens exposed to other treatments. The plasma caeruloplasmin concentration in chickens fed a 0.001% 5-ALA-supplemented diet was significantly lower than in controls or in chickens fed diets supplemented with other concentrations of 5-ALA 24 h after injection of LPS. In addition, BW at 21 and 50 d of age was significantly higher in chickens fed a 0.001% 5-ALA-supplemented diet than in control chickens. The findings suggest that supplementation of diets with 0.001% 5-ALA could prevent the catabolic changes induced by immunological stimulation. These results show that 5-ALA might be useful as an immunomodulator to stimulate T-cells via mild oxidative stress in growing broiler chickens, thereby improving the growth performance.

Hydroxytyrosol Attenuates Peripheral Neuropathy in Streptozotocin-Induced Diabetes in Rats

Peripheral neuropathy is one of the most frequent and severe complications of diabetes. Hydroxytyrosol (HT), the major antioxidant polyphenolic compound of olive oil, has been investigated as a new potential treatment to counteract the progression of peripheral diabetic neuropathy in rats. An established model of streptozotocin-induced diabetes has been used. After confirmation of hyperglycemia, diabetic and nondiabetic animals were randomized to receive either a low dose or a high dose of HT, or the corresponding vehicle, for 6 weeks. At the end of the 6-week period of treatment, HT blunted plasma thiobarbituric acid-reactive substances increase (p < 0.05) and significantly reduced nerve conduction velocity (p < 0.05) and thermal nociception impairment in diabetic rats (p < 0.05). Sciatic nerve Na(+), K(+)-ATPase activity reduction was also abolished by HT (p < 0.05). The present study provides evidence of the therapeutic potential of the natural substance hydroxytyrosol in the early stage of diabetic neuropathy.

The physiological stress response to high-intensity sprint exercise following the ingestion of sodium bicarbonate

The purpose of this study was to investigate the effects of pre-exercise alkalosis on the physiological stress response to high-intensity exercise. Seven physically active males (age 22 ± 3 years, height 1.82 ± 0.06 m, mass 81.3 ± 8.4 kg and peak power output 300 ± 22 W) performed a repeated sprint cycle exercise following a dose of 0.3 g kg(-1) body mass of sodium bicarbonate (NaHCO(3)) (BICARB), or a placebo of 0.045 g kg(-1) body mass of sodium chloride (PLAC). Monocyte-expressed heat shock protein 72 (HSP72) and plasma thiobarbituric acid reactive substances (TBARS) were significantly attenuated in BICARB compared to PLAC (p = 0.04 and p = 0.039, respectively), however total anti-oxidant capacity, the ratio of oxidised to total glutathione, cortisol, interleukin 6 and interleukin 8 were not significantly induced by the exercise. In conclusion, monocyte-expressed HSP72 is significantly increased following high-intensity anaerobic exercise, and its attenuation following such exercise with the ingestion of NaHCO(3) is unlikely to be due to a decreased oxidative stress.

High-intensity exercise attenuates postprandial lipaemia and markers of oxidative stress

Regular exercise can reduce the risk of CVD (cardiovascular disease). Although moderate-intensity exercise can attenuate postprandial TAG (triacylglycerol), high-intensity intermittent exercise might be a more effective method to improve health. We compared the effects of high-intensity intermittent exercise and 30min of brisk walking on postprandial TAG, soluble adhesion molecules and markers of oxidative stress. Nine men each completed three 2-day trials. On day 1, subjects rested (control), walked briskly for 30min (walking) or performed 5×30s maximal sprints (high-intensity). On day 2, subjects consumed a high-fat meal for breakfast and 3h later for lunch. Blood samples were taken at various times and analysed for TAG, glucose, insulin, ICAM-1 (intracellular adhesion molecule-1), VCAM-1 (vascular adhesion molecule-1), TBARS (thiobarbituric acid- reactive substances), protein carbonyls and β-hydroxybutyrate. On day 2 of the high-intensity trial, there was a lower (P<0.05) incremental TAG AUC (area under the curve; 6.42±2.24mmol/l per 7h) compared with the control trial (9.68±4.77mmol/l per 7h) with no differences during day 2 of the walking trial (8.98±2.84mmol/l per 7h). A trend (P=0.056) for a reduced total TAG AUC was also seen during the high-intensity trial (14.13±2.83mmol/l per 7h) compared with control (17.18±3.92mmol/l per 7h), walking showed no difference (16.33±3.51mmol/l per 7h). On day 2 of the high-intensity trial plasma TBARS and protein carbonyls were also reduced (P<0.05) when compared with the control and walking trials. In conclusion, high-intensity intermittent exercise attenuates postprandial TAG and markers of oxidative stress after the consumption of a high-fat meal.

Hyperandrogenism Sensitizes Leukocytes to Hyperglycemia to Promote Oxidative Stress in Lean Reproductive-Age Women

Hyperandrogenism and oxidative stress are related in polycystic ovary syndrome (PCOS), but it is unknown whether hyperandrogenemia can activate oxidative stress. The purpose of this study was to determine the effect of oral androgen administration on fasting and glucose-stimulated leukocytic reactive oxygen species (ROS) generation, reduced nicotinamide adenine dinucleotide phosphate oxidase p47(phox) subunit gene expression, and plasma thiobarbituric acid-reactive substances (TBARS) in lean healthy reproductive-age women. Sixteen lean healthy ovulatory reproductive-age women were treated with 130 mg dehydroepiandrosterone (DHEA) or placebo (n = 8 each) for 5 d in this randomized, controlled, double-blind study that was performed at an an academic medical center. Leukocytic ROS generation, p47(phox) gene expression, and plasma TBARS were quantified in the fasting state and 2 h after glucose ingestion, before and after treatment. Before treatment, subjects receiving DHEA or placebo exhibited no differences in androgens or any prooxidant markers while fasting and after glucose ingestion. Compared with placebo, DHEA administration raised levels of testosterone, androstenedione, and DHEA-sulfate, increased the percent change in glucose-challenged p47(phox) RNA content, and increased the percent change in fasting and glucose-challenged ROS generation from mononuclear cells and polymorphonuclear cells, p47(phox) protein content, and plasma TBARS. Elevation of circulating androgens comparable to what is present in PCOS increases leukocytic ROS generation, p47(phox) gene expression, and plasma TBARS to promote oxidative stress in lean healthy reproductive-age women. Thus, hyperandrogenemia activates and sensitizes leukocytes to glucose in this population.

Quercetin in Dimethyl Benzanthracene Induced Breast Cancer in Rats

Problem statement: Vincristine a commonly used anticancer agent in th e treatment of breast cancer results in serious adverse effects li ke teratogenicity, neurotoxicity and carcinogenicit y on long term use. Drug resistance is also a common pro blem encountered with vincristine. Hence the effect of flavonol quercetin, a known antioxidant w ith no known documented adverse effect was tried in treatment of DMBA induced breast cancer in female rats and its effect was compared with vincristine. Approach: Quercetin at the dose of 50, 100-200 mg kg -1 body weight was administered in DMBA induced breast cancer in female wistar rats and its effects were compared with Vincristine. The anti oxidant enzymes, catalase, glutathione peroxid ase and superoxide dismutase and Thiobarbituric Acid Reactive Substances (TBARS) level in cancerous breast tissue, TBARS and catalase in plasma and superoxide dismutase and glutathione peroxidase in erythrocyte lysate were estimated. Results: Quercetin supplementation at the dose of 100 mg kg -1 body weight was most effective in alleviating cancer symptoms and was comparable to vincristine. The plasma TBARS were reduced and breast tissue TBARS were elevated. The antioxidant enzymes were rejuvenated by quercetin supplementation at all three dose levels. Conclusion: Quercetin is found to be an effective chemotherape utic agent in the treatment of breast cancer on par with vincrist ine. Being a plant product, quercetin can also be u sed in chemoprophylaxis in high risk individuals with g enetic predisposition towards breast cancer. Besides, it can be given orally and has a wide marg in of safety.

N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation

Sepsis is a common cause of acute kidney injury (AKI) and acute lung injury. Oxidative stress plays as important role in such injury. The aim of this study was to evaluate the effects that the potent antioxidant N-acetylcysteine (NAC) has on renal and pulmonary function in rats with sepsis. Rats, treated or not with NAC (4.8 g/l in drinking water), underwent cecal ligation and puncture (CLP) 2 days after the initiation of NAC treatment, which was maintained throughout the study. At 24 h post-CLP, renal and pulmonary function were studied in four groups: control, control + NAC, CLP, and CLP + NAC. All animals were submitted to low-tidal-volume mechanical ventilation. We evaluated respiratory mechanics, the sodium cotransporters Na-K-2Cl (NKCC1) and the α-subunit of the epithelial sodium channel (α-ENaC), polymorphonuclear neutrophils, the edema index, oxidative stress (plasma thiobarbituric acid reactive substances and lung tissue 8-isoprostane), and glomerular filtration rate. The CLP rats developed AKI, which was ameliorated in the CLP + NAC rats. Sepsis-induced alterations in respiratory mechanics were also ameliorated by NAC. Edema indexes were lower in the CLP + NAC group, as was the wet-to-dry lung weight ratio. In CLP + NAC rats, α-ENaC expression was upregulated, whereas that of NKCC1 was downregulated, although the difference was not significant. In the CLP + NAC group, oxidative stress was significantly lower and survival rates were significantly higher than in the CLP group. The protective effects of NAC (against kidney and lung injury) are likely attributable to the decrease in oxidative stress, suggesting that NAC can be useful in the treatment of sepsis.

Protandim does not influence alveolar epithelial permeability or intrapulmonary oxidative stress in human subjects with alcohol use disorders

Alcohol use disorders (AUDs), including alcohol abuse and dependence, have been linked to the development of acute lung injury (ALI). Prior clinical investigations suggested an association between AUDs and abnormal alveolar epithelial permeability mediated through pulmonary oxidative stress that may partially explain this relationship. We sought to determine if correcting pulmonary oxidative stress in the setting of AUDs would normalize alveolar epithelial permeability in a double-blinded, randomized, placebo-controlled trial of Protandim, a nutraceutical reported to enhance antioxidant activity. We randomized 30 otherwise healthy AUD subjects to receive directly observed inpatient oral therapy with either Protandim (1,350 mg/day) or placebo. Subjects underwent bronchoalveolar lavage (BAL) and blood sampling before study drug administration and after 7 days of therapy; all AUD subjects completed the study protocol without adverse events. BAL total protein was measured at each timepoint as an indicator of alveolar epithelial permeability. In subjects with AUDs, before study drug initiation, BAL total protein values were not significantly higher than in 11 concurrently enrolled controls (P = 0.07). Over the 7-day study period, AUD subjects did not exhibit a significant change in BAL total protein, regardless of their randomization to Protandim {n = 14, -2% [intraquartile range (IQR), -56-146%]} or to placebo [n = 16, 77% (IQR -20-290%); P = 0.19]. Additionally, among those with AUDs, no significant changes in BAL oxidative stress indexes, epithelial growth factor, fibroblast growth factor, interleukin-1β, or interleukin-10 were observed regardless of drug type received. Plasma thiobarbituric acid reactive substances, a marker of lipid peroxidation, decreased significantly over time among AUD subjects randomized to placebo (P < 0.01). These results suggest that Protandim for 7 days in individuals with AUDs who are newly abstinent does not alter alveolar epithelial permeability. However, our work demonstrates the feasibility of safely conducting clinical trials that include serial bronchoscopies in a vulnerable population at risk for acute lung injury.

Maternal Prolactin Inhibition during Lactation Affects Physical Performance Evaluated by Acute Exhaustive Swimming Exercise in Adult Rat Offspring

Maternal prolactin inhibition at the end of lactation programs for metabolic syndrome and hypothyroidism in adult offspring, which could negatively affect exercise performance. We evaluated the effects of maternal hypoprolactinemia in late lactation on physical performance in adult progeny. Lactating Wistar rats were treated with bromocriptine (BRO, 1 mg per day) or saline on days 19, 20, and 21 of lactation and offspring were followed until 180 days old. Physical performance was recorded in untrained rats at 90 and 180 days by an acute exhaustive swimming test (exercise group-Ex). At day 90, BRO offspring showed higher visceral fat mass, higher plasma thiobarbituric acid reactive substances, lower total antioxidant capacity, higher liver glycogen, lower glycemia, and normal insulinemia. Although thyroid hormones (TH) levels were unchanged, mitochondrial glycerol phosphate dehydrogenase (mGPD) activity was lower in muscle and in brown adipose tissue (BAT). At this age, BRO-Ex offspring showed higher exercise capacity, lower blood lactate, higher serum T3, and higher muscle and BAT mGPD activities. At day 180, BRO offspring showed central obesity, hypothyroidism, insulin resistance, and lower EDL (extensor digitorum longus) muscle glycogen with unaltered plasma oxidative stress markers. This group showed no alteration of exercise capacity or blood lactate. After exercise, EDL and liver glycogen were lower, while T3 levels, BAT and muscle mGPD activities were normalized. Liver glycogen seem to be related with higher exercise capacity in younger BRO offspring, while the loss of this temporary advantage maybe related to the hypothyroidism and insulin resistance developed with age.

Oxidative Stress Markers in Prostate Cancer Patients after HDR Brachytherapy Combined with External Beam Radiation

Assessment of oxidative stress markers was perfomed in prostate cancer (PCa) patients subjected to high-dose brachytherapy (HDR) with external beam radiotherapy (EBRT). Sixty men with PCa were subjected to combined two-fraction treatment with HDR (tot. 20 Gy) and EBRT (46 Gy). Blood samples were taken before treatment, immediately afterwards, after 1.5–3 months, and approx. 2 years. Control group consisted of 30 healthy men. Erythrocyte glutathione peroxidase activity in the patients was lower than in healthy subjects by 34% (P < 0.001), 50% (P < 0.001), 30% (P < 0.05), and 61% (P < 0.001), respectively, at all periods. No significant differences were found by comparing superoxide dismutase and catalase activity in PCa patients with that of the controls. After 2 years of the end of treatment, the activity of studied enzymes demonstrated a decreasing tendency versus before therapy. Blood plasma thiobarbituric acid reactive substances (TBARS) concentration was higher than in the controls at all periods, while erythrocyte TBARS decreased after 2 years to control levels. The results confirm that in the course of PCa, imbalance of oxidant-antioxidant processes occurs. The therapy did not alter the levels of oxidative stress markers, which may prove its applicability. Two years is too short a period to restore the oxidant-antioxidant balance.

Mate Tea Prevents Oxidative Stress in the Blood and Hippocampus of Rats with Acute or Chronic Ethanol Administration

Objective. The aim of this study was to evaluate the influence of acute and chronic intake of mate tea on the effects elicited by acute and chronic administration of ethanol. Methods. Oxidative stress was evaluated by measuring thiobarbituric acid-reactive substances (TBARS), as well as the activities of the antioxidant enzymes, catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in the hippocampus and blood of rats. Male Wistar rats were randomly assigned to four groups, for both acute and chronic treatment: (1) control group, (2) treated group, (3) intoxicated group, (4) and intoxicated group treated with mate tea. Results. Both ethanol administrations significantly increased TBARS in plasma and hippocampus of rats and altered antioxidant enzyme activities, changes which were reverted by mate tea administration. Conclusions. Data indicate that acute and chronic ethanol administration induced oxidative stress in hippocampus and blood and that mate tea treatment was able to prevent this situation.

The Oxidative Stress in Cataract Patients

The recent studies on cataract formation focus on the primary role of the systemic oxidative stress which is generated outside the lens. Our research was directed to assess the oxidative stress by measuring the lipid peroxidation products in the form of the Thiobarbituric Acid Reactive Substances (TBARS) and the antioxidant enzyme levels in the blood. The antioxidant therapy may have a role to play in delaying the onset and the progression of age related cataracts. This was a case control study. It comprised of 100 age matched subjects (50 with cataracts and 50 controls) with their ages ranging from 45- 75 years. Oxidative stresses such as the Thiobarbituric Acid Reactive Substances (TBARS) and the antioxidant enzymes, Superoxide Dismutase (SOD) and Glutathione Peroxidase( GPX ) were investigated in all the patients and the controls. Significantly increased levels of serum lipid peroxide in the form of Malondialdehyde (MDA) (p<0.001) were observed in the cataract patients as compared to the controls. Significantly decreased blood levels of SOD and GPX were observed in all the patients. In the present study, it was concluded that oxidative stress plays an important role in the onset and the progression of cataracts. The pro-oxidant i.e. serum malondialdehyde (MDA) levels were increased in the cataract patients. The blood levels of the enzymatic anti-oxidants, SOD and GPX were decreased. The plasma TBARS can be used as biomarkers of the degeneration in the lens.

Does Dialysis Modality Influence the Oxidative Stress of Uremic Patients?

Background/Aims: Since peritoneal membrane is more compatible and residual renal function better preserved during peritoneal dialysis, we questioned whether the oxidative burden in chronic kidney disease (CKD) is influenced by dialysis modality. Methods: 49 stable CKD patients, 17 on continuous ambulatory peritoneal dialysis (CAPD), 16 on hemodialysis (HD), and 16 non-dialyzed, and 13 healthy subjects were enrolled. Plasma thiobarbituric acid-reactive substances (TBARS; nmol/g protein), serum total antioxidant activity (TAA), total plasma-free thiols (Pt-SH; µmol/g protein), albumin and uric acid were measured by spectrophotometry. Serum residual antioxidant activity (RAA) was calculated. Results: TBARS were higher in HD (78.3 ± 20.3) versus both non-dialyzed (53.1 ± 27.9, p = 0.007) and CAPD groups (58.3 ± 19.8, p = 0.008). Pt-SH was reduced in CKD patients, but showed comparable values between dialysis groups. TAA and RAA were similarly increased in HD and CAPD patients than in the other two groups. Conclusion: Oxidative stress occurs in all CKD patients and worsens as renal function declines. Lipid peroxidation seems more augmented during chronic HD as compared to CAPD, but the plasma antioxidant status did not differ between the investigated dialysis methods. Therefore, dialysis modality appears to influence lipid peroxidation without changing the extracellular antioxidant defense of CKD patients.