AIM:To detect the effects of verbascoside on decreasing the concentration of oxygen free radicals (OFR) and lipid peroxidation in skeletal muscle resulting from exhaustive exercise.

METHODS:Electron spin resonance (ESR) technique and thiobarbituric acid reaction (TBAR) method were used to detect the concentration of OFR in intact gastrocnemius muscle and the contents of milondialdehyde (MDA) in muscle homogenate.

RESULTS:Verbascoside decreased the concentration of OFR (P<0.05) and the level of lipid peroxidation (P<0.05) in muscle caused by exercise.

CONCLUSION:Verbascoside has the effects of reducing oxidative stress in muscle caused by exhaustive exercise by decreasing the concentration of free radicals and the level of lipid peroxidation.

Periodontitis is a disease, which is associated with chronic inflammation and leads to significant destruction of periodontal tissues. Periodontal ligament cells (PDLCs) constitute the largest cell population in PDL tissues and a considerable body of evidence has demonstrated an association between oxidative stress and the progression of periodontitis. However, the effects on PDLCs exposed to hydrogen peroxide (H2O2) and the molecular mechanisms by which H2O2 affects periodontitis remain to be elucidated. In the present study, the potential cytotoxic effect of H2O2 and the antioxidative function of vitamin C (Vc) in PDLCs were investigated. The results demonstrated that H2O2 treatment decreased the viability of PDLCs. The decreased PDLC viability was primarily induced by apoptosis, which was evidenced by cleaved caspases-3, caspases-9 and poly (ADP-ribose) polymerase. Following optimal Vc addition, the proapoptotic effects of H2O2 were partially antagonized. Taken together, the present study demonstrated that H2O2 primarily induced the apoptosis of PDLCs and that these adverse effects were partially rescued following treatment with Vc. These results revealed how H2O2 promotes the progression of periodontitis and provide an improved understanding of the reversal effect of antioxidant treatment. Therefore, optimal Vc administration may provide a potentially effective technique in periodontal therapy.

INTRODUCTION:Etomidate is usually preferred in the induction of cardiac compromised patients due to its relative cardiovascular stability. However, the use of this drug has been limited as etomidate induces suppression of cortisol biosynthesis as a result of blockade of 11-beta-hydroxylation in the adrenal gland, mediated by the imidazole radical of etomidate. This study was carried out to observe the effect of Vitamin C on adrenal suppression after etomidate induction in patients undergoing cardiac surgery.

MATERIALS AND METHODS:A total of 78 patients were randomly distributed into two groups. Group-I received oral Vitamin C (500 mg) twice daily and Group-II received antacid tablet as placebo twice daily instead of Vitamin C for 7 consecutive days prior to surgery till morning of surgery. Patients of both the groups induced with etomidate (0.1-0.3 mg/kg). Blood cortisol was estimated at different points of time till 24 th postinduction hour/blood lactate, glucose, hemodynamic parameters, and perioperative outcomes were assessed.

RESULTS:Data of seventy patients (n = 35 in each group) were finally analyzed. Cortisol level is statistically significantly higher in Group-I (69.51± 7.65) as compared to Group-II (27.74 ± 4.72) (P<0.05) in the 1 st postinduction hour. In Group-II, cortisol was consistently lower for 1 st 24 postinduction hour. Total adrenaline requirement was statistically significantly high in Group-II. Time of extubation, length of Intensive Care Unit stay arrhythmia was similar in both the groups.

CONCLUSION:Vitamin C effectively inhibits etomidate-induced adrenal suppression in cardiac patients, thereby etomidate can be used as a safe alternative for induction in cardiac surgery under cardiopulmonary bypass when pretreated with Vitamin C.

BACKGROUND:The pathogenesis of reflex sympathetic dystrophy (RSD) is not clear, nor is there a definitive treatment for this syndrome. The morbidity, costs in health care, and loss of work time justify the search for a means to prevent post-traumatic dystrophy. Although the role of toxic oxygen radicals has not yet been clarified, we investigated vitamin C (ascorbic acid) as a prophylactic antioxidant drug.

METHODS:123 adults with 127 conservatively treated wrist fractures were randomly allocated in a double-blind trial to take a capsule of 500 mg vitamin C or placebo daily for 50 days. Each participant's sex, age, side of fracture, dominance, fracture type, dislocation, reduction, and complaints with the plaster cast were recorded, and they were clinically scored for RSD. The follow-up lasted 1 year.

FINDINGS:Eight patients were withdrawn after randomisation. 52 patients with 54 fractures (male 22%, female 78%; mean age 57 years) received vitamin C and 63 patients with 65 fractures (male 20%, female 80%; mean age 60 years) received placebo. RSD occurred in four (7%) wrists in the vitamin C group and 14 (22%) in the placebo group 15% (95% CI for differences 2-26). Other significant prognostic variables for the occurrence of RSD were complaints while wearing the cast (relative risk 0.17 [0.07-0.41]) and fracture type (0.37 [0.16-0.89]).

INTERPRETATION:This prospective, double-blind study shows that vitamin C was associated with a lower risk of RSD after wrist fractures. Our hypothesis is that this beneficial effect of prophylaxis would be useful in other forms of trauma.

BACKGROUND:Obesity is well associated as being an interfering factor in metabolic diseases such as hypertension and diabetes by increasing the secretion of proinflammatory markers from adipose tissue. Having healthy effects, vitamin C could work as an anti-inflammatory agent through its antioxidant capacity.

REGISTRATION:

REGISTRATION NUMBER:FPSK_Mac [13]04.

OBJECTIVE:The aim of the study reported here was to identify the effect of vitamin C on reducing the levels of inflammatory markers in hypertensive and/or diabetic obese adults.

SUBJECTS AND METHODS:Sixty-four obese patients, who were hypertensive and/or diabetic and had high levels of inflammatory markers, from primary health care centers in Gaza City, Palestine, were enrolled into one of two groups in an open-label, parallel, randomized controlled trial. A total of 33 patients were randomized into a control group and 31 patients were randomized into an experimental group. The experimental group was treated with 500 mg vitamin C twice a day.

RESULTS:In the experimental group, vitamin C significantly reduced the levels of high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), fasting blood glucose (FBG), and triglyceride (TG) after 8 weeks of treatment (overall: P<0.001); no changes appeared in total cholesterol (TC). In the control group, there were significant reductions in FBG and TG (P=0.001 and P=0.026, respectively), and no changes in hs-CRP, IL-6, or TC. On comparing the changes in the experimental group with those in the control group at the endpoint, vitamin C was found to have achieved clinical significance in treating effectiveness for reducing hs-CRP, IL-6, and FBG levels (P=0.01, P=0.001, and P<0.001, respectively), but no significant changes in TC or TG were found.

CONCLUSION:Vitamin C (500 mg twice daily) has potential effects in alleviating inflammatory status by reducing hs-CRP, IL-6, and FBG in hypertensive and/or diabetic obese patients.

AIM:Hypothetically, supplementation with the antioxidant vitamins C could alleviate exercise-induced lipid peroxidation. The purpose of this study was to evaluate the effect of vitamin C supplementation on exercise-induced lipid peroxidation, muscle damage and inflammation.

METHODS:Sixteen healthy untrained male volunteers participated in a 30-min exercise at 75% Vo2max. Subjects were randomly assigned to one of two groups: 1) placebo and 2) vitamin C (VC: 1 000 mg vitamin C). Blood samples were obtained prior to supplementation (baseline), 2 h after supplementation (immediately pre-exercise), post-exercise, 2 and 24 h after exercise. Plasma levels of VC, total antioxidant capacity (TAC), creatine kinase (CK), malondealdehyde (MDA), total leukocytes, neutrophils, lymphocytes, interleukin-6 (IL-6) and cortisol were measured.

RESULTS:Plasma vitamin C concentrations increased significantly in the VC in response to supplementation and exercise (P<0.05). TAC decreased significantly in Placebo group 24 h after exercise compared to pre-exercise (P<0.05). Although MDA levels were similar between groups at baseline, it increased significantly 2 h after exercise only in the Placebo group (P<0.05). CK increased immediately and 2 h after exercise in both groups and 24 h after exercise only in placebo group compared to pre-exercise (P<0.05). Markers of inflammation (total leukocyte counts, neutrophil counts and IL-6) were increased significantly in response to the exercise (P<0.05). In VC group, there was significant increase in lymphocyte counts immediately after exercise compared with pre-exercise (P<0.05). Serum cortisol concentrations significantly declined after supplementation compared with baseline (P<0.05) as well as declined 2 and 24 h after exercise compared with immediately after exercise in VC group (P<0.05).

CONCLUSION:VC supplementation prevented endurance exercise-induced lipid peroxidation and muscle damage but had no effect on inflammatory markers.

BACKGROUND AND OBJECTIVES:Evidence suggests associations between vitamin D deficiency and cardiovascular disease (CVD) risk factors, including hypertension and excessive cortisol levels. Also, vitamin D levels may impact exercise performance. Thus, we aimed to investigate the effects of vitamin D intake on cardiovascular risk factors, free urinary cortisol and exercise performance.

METHODS:A randomized placebo-controlled single-blinded parallel trial was conducted in healthy participants (n = 15). They received 2000 IU (50µg) vitamin D3 per day (n = 9) or placebo (lactose) (n = 6) for 14 days. Body composition, systolic blood pressure (SBP), diastolic blood pressure (DBP) and arterial elasticity (as measured by pulse wave velocity, PWV) were recorded at baseline, day 7 and day 14 of intervention. A total of two 24-hour urine samples were collected to estimate free cortisol and cortisone levels. Exercise performance was assessed at the baseline and day 14 of the intervention using a bike ergometer in which BP and PWV were measured before and after exercise. The distance cycled in 20 minutes and the Borg Scale rate of perceived exertion (RPE) were recorded.

RESULTS:In the intervention arm, at day 14, vitamin D supplementation significantly reduced SBP and DBP from 115.8± 17.1 and 75.4 ± 10.3 at baseline to 106.3 ± 10.9 (p = 0.022) and 68.5 ± 10.1 mmHg (p = 0.012) respectively. Also arterial stiffness was markedly reduced in the vitamin D group (from 7.45 ± 1.55 to 6.11 ± 1.89, p = 0.049). Urinary free cortisol levels and cortisol/cortisone ratio were significantly reduced from 162.65 ± 58.9 nmol/day and 2.22 ± 0.7 to 96.4 ± 37.2 (p = 0.029) and 1.04 ± 0.4 (p = 0.017) respectively. Exercise-induced SBP and DBP were significantly reduced post vitamin D intake from 130.7 ± 12.2 to 116.1 ± 8.1 (p = 0.012) and from 76.2 ± 8.4 to 70.5 ± 7.7 mmHg (p =0.042) respectively. The distance cycled in 20 minutes significantly increased from 4.98 ± 2.65 to 6.51 ± 2.28km (p = 0.020), while the Borg Scale RPE reduced from 5.13 ± 1.36 to 4.25 ± 0.71 RPE (p = 0.021). In the placebo arm, no significant effects on CVD risk factors and exercise performancewere observed.

CONCLUSION:These results suggest that daily vitamin D supplementation may ameliorate CVD risk factors including a decrease in 11β-HSD1 activity, as evidenced by the decrease in the cortisol/cortisone ratio, and improve exercise performance in healthy individuals. However, large scale studies are required to verify our findings.

OBJECTIVE:To determine whether vitamins C and E supplementation lowers oxidative stress marker levels and improves pregnancy rate in women with endometriosis.

METHODS:Thirty-four women with endometriosis received a bar containing vitamins C and E (343 mg and 84 mg, respectively) or placebo for 6 months. Plasma and peritoneal fluid levels of malondialdehyde (MDA) and lipid hydroperoxides (LOOHs) were measured for all women and compared between the 2 groups. Data were analyzed by the t test or 1-way analysis of variance for parametric data and the Mann-Whitney rank sum test or Kruskall-Wallis test for nonparametric data. The Fisher exact test was used to compare pregnancy rates.

RESULTS:After 4 months, the study group had lower levels of MDA and LOOHs than the control group, and the difference became statistically significant in the fourth month for MDA levels and in the sixth month for LOOH levels. The postintervention pregnancy rates were 19% and 12% in the supplementation and placebo groups, respectively, but the difference was not significant.

CONCLUSIONS:Vitamins C and E supplementation was associated with a decrease in the concentration of oxidative stress markers in women with endometriosis. The pregnancy rate, however, did not improve during or after the intervention.

BACKGROUND:Oxidative stress promotes endothelial dysfunction and atherosclerosis in chronic renal disease.

OBJECTIVES:This study investigated the impact of Hatha yoga on oxidative stress indicators and oxidant status, in patients with end-stage renal disease (ESRD) on hemodialysis.

DESIGN:This prospective randomized study consisted of 33 ESRD patients in the Hatha yoga exercise group who were matched with 35 ESRD patients in the control group.

OUTCOME MEASURES:The oxidative stress indicators (malondialdehyde - MDA, protein oxidation - POX, phospholipase A2 - PLA2 activity) and the oxidative status (superoxide dismutase (SOD) and catalase activities) were determined in the blood samples taken at the pre-hemodialysis treatment, at baseline (0 months) and after four months.

RESULTS:In patients in the Hatha yoga exercise group, lipid peroxidation, as indicated by MDA decreased by 4.0% after four months (P = 0.096). There was also a significant reduction in the activity of PLA from 2.68± 0.02 IU / L to 2.34 IU / L (- 12.7%; P = 0.010) and POX from 2.28 ± 0.02 nmol / mg to 2.22 ± 0.01 nmol / mg (- 22.6%; P = 0.0001). The activity of SOD significantly increased from 12.91 ± 0.17 U / L to 13.54 ± 0.15 U / L (4.65%; P = 0.0001) and catalase from 79.83 ± 0.63 U / L to 80.54 ± 0.80 U / L (0.90%; P = 0.0001). There was a significant correlation between the pre-hemodialysis oxidative stress parameters at the zero month and after four months for the activities of PLA (r = 0.440), catalase (r = 0.872), and SOD (r = 0.775).

CONCLUSIONS:These findings suggest that the Hatha yoga exercise has therapeutic, preventative, and protective effects in ESRD subjects, by decreasing oxidative stress.

PURPOSE:This study tested the effectiveness of a fruit, berry, and vegetable concentrate (FVC), Juice Plus+® (NSA LLC, Collierville, TN), supplement on muscle function and oxidative stress in response to an acute bout of eccentric exercise (EE).

METHODS:Forty-one healthy volunteers (age = 18-35 yr) were randomly assigned to either a placebo (P) or an FVC treatment taking capsules for 28 d (6 d(-1)) before EE and for the next 4 d. All subjects completed four sets of 12 repetitions of eccentric elbow flexion with their nondominant arm. Blood, muscle soreness (MS), range of motion (ROM), and maximal isometric force (MIF) of the elbow flexors were obtained before and immediately after exercise and at 2, 6, 24, 48, and 72 h postexercise. Plasma was analyzed for creatine kinase (CK), lipid hydroperoxides, malondialdehyde (MDA), and protein carbonyls (PC). Glutathione ratio was determined from whole-blood extracts.

RESULTS:MS, ROM, MIF, and plasma CK demonstrated significant time effects independent of treatment. MS and plasma CK increased over time, whereas ROM and MIF decreased over time. There was a significant time and time× treatment effect for plasma PC and MDA. PC and MDA increased over time in the P group (P<0.01) but were not significantly altered in the FVC-treated group at any time. No significant changes were noted in lipid hydroperoxides. The glutathione ratio was elevated immediately postexercise in both groups (P<0.01) and elevated 6 h postexercise with P compared with the FVC-treated group (P<0.05).

CONCLUSION:This study reports that 4 wk of pretreatment with an FVC can attenuate blood oxidative stress markers induced by EE but had no significant impact on the functional changes related to pain and muscle damage.

AIM:The aim of this study was to investigate the effect of acute L-carnitine supplementation at two different doses on nitric oxide (NO) production and oxidative stress after exhaustive exercise.

METHODS:The subjects were 26 healthy males aged 17-19 years. Subjects were randomly divided into two groups of 13 each and received 3 or 4 g L-carnitine via a glass of fruit juice. After 1 h, the treadmill test was started at a speed of 8 km/h, afterwards increasing the speed 1 km/h every 3 min with a 1 min rest before every speed increase until exhaustion. Venous blood samples were collected again within 5 min following the exercise test. One week later, the test was repeated on the same athletes with placebo fluids. All subjects received a placebo via a glass of fruit juice. 1 h after the same exercise protocol mentioned above was performed and blood samples were drawn immediately. These plasma samples were used for measurement of nitrate-nitrite (NOx), which are known to be the stable end products of NO, TBARs as a lipid peroxidation indicator and an antioxidant glutathione (GSH) levels.

RESULTS AND CONCLUSION:The results of this study have shown that L-carnitine applied at a 3 g dose provides strong antioxidant action by increasing the GSH and NOx level and decreasing the TBARs level.

Reactive oxygen species (ROS) are elevated by metabolic changes in diabetes, including autoxidation and increased advanced glycation. Endogenous protection by the glutathione redox cycle is also compromised by the competing NADPH requirement of elevated polyol pathway flux. Antioxidant treatment strategies prevent or reverse nerve conduction velocity (NCV) deficits in diabetic rats. These include lipophilic scavengers such as butylated hydroxytoluene, probucol and vitamin E, more hydrophilic agents like alpha-lipoic acid and acetyl cysteine, and transition metal chelators that inhibit autoxidation. In the long-term, elevated ROS cause cumulative damage to neurons and Schwann cells, however, they also have a deleterious effect on nerve blood flow in the short term. This causes endoneurial hypoxia, which is responsible for early NCV deficits. Antioxidant treatment corrects the blood flow deficit and promotes normal endoneurial oxygenation. ROS cause antioxidant-preventable vascular endothelium abnormalities, neutralizing nitric oxide mediated vasodilation and increasing reactivity to vasoconstrictors. Unsaturated fatty acids are a major target for ROS and essential fatty acid metabolism is impaired by diabetes. Gamma-linolenic acid stimulates vasodilator prostanoid production, and there are marked synergistic interactions between gamma-linolenic acid and antioxidants. This has encouraged the development of novel drugs such as ascorbyl-gamma-linolenic acid and gamma-linolenic acid-lipoic acid with enhanced therapeutic potential.

Alzheimer's disease (AD) is a neurodegenerative disease, in which the primary etiology remains unknown. AD presents amyloid beta (Aβ) protein aggregation and neurofibrillary plaque deposits. AD shows oxidative stress and chronic inflammation. In AD, canonical Wingless-Int (Wnt)/β-catenin pathway is downregulated, whereas peroxisome proliferator-activated receptor γ (PPARγ) is increased. Downregulation of Wnt/β-catenin, through activation of glycogen synthase kinase-3β (GSK-3β) by Aβ, and inactivation of phosphatidylinositol 3-kinase/Akt signaling involve oxidative stress in AD. Cannabidiol (CBD) is a non-psychotomimetic phytocannabinoid from Cannabis sativa plant. In PC12 cells, Aβ-induced tau protein hyperphosphorylation is inhibited by CBD. This inhibition is associated with a downregulation of p-GSK-3β, an inhibitor of Wnt pathway. CBD may also increase Wnt/β-catenin by stimulation of PPARγ, inhibition of Aβ and ubiquitination of amyloid precursor protein. CBD attenuates oxidative stress and diminishes mitochondrial dysfunction and reactive oxygen species generation. CBD suppresses, through activation of PPARγ, pro-inflammatory signaling and may be a potential new candidate for AD therapy.

The purpose of this study was to investigate the effects of curcumin supplementation on exercise-induced oxidative stress in humans. 10 male participants, ages 26.8±2.0 years (mean±SE), completed 3 trials in a random order: (1) placebo (control), (2) single (only before exercise) and (3) double (before and immediately after exercise) curcumin supplementation trials. Each participant received oral administration of 90 mg of curcumin or the placebo 2h beforeexercise and immediately after exercise. Each participant walked or ran at 65% of V˙2max on a treadmill for 60min. Blood samples were collected pre-exercise, immediately after exercise and 2h after exercise. The concentrations of serum derivatives of reactive oxygen metabolites measured immediately after exercise were significantly higher than pre-exercise values in the placebo trial (308.8±12.9 U. CARR, P<0.05), but not in the single (259.9±17.1 U. CARR) or double (273.6±19.7 U. CARR) curcumin supplementation trials. Serum biological antioxidant potential concentrations measured immediately after exercise were significantly elevated in the single and double curcumin supplementation trials compared with pre-exercise values (P<0.05). These findings indicate that curcumin supplementation can attenuate exercise-induced oxidative stress by increasing blood antioxidant capacity.

CONTEXT: Limited information exists on the interaction between diet and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) and the interaction's effect on serum lipid and lipoprotein levels, insulin sensitivity, and circulating antioxidant vitamin and provitamin levels. OBJECTIVE: To evaluate the separate and combined effects of diet and simvastatin therapy on serum levels of lipids, lipoproteins, antioxidants, and insulin.

DESIGN, SETTING, AND PARTICIPANTS: Randomized, controlled crossover trial conducted from August 1997 to June 1998 in 120 previously untreated hypercholesterolemic men aged 35 to 64 years who were recruited from the community in Turku, southwestern Finland.

INTERVENTIONS: After a 4- to 6-week placebo run-in period, participants were randomly allocated to a habitual diet (n = 60) or dietary treatment group (n = 60), and each of these groups was further randomized in a double-blind crossover fashion to receive simvastatin (20 mg/d) or placebo, each for 12 weeks (n = 30 in each group). The main goals of the dietary treatment were to reduce energy intake from saturated plus trans-unsaturated fats to no more than 10% by replacing them partly with monounsaturated and polyunsaturated fats rich in omega-3 fatty acids and to increase intake of fruits, vegetables, and dietary fiber.

MAIN OUTCOME MEASURES: Changes in levels of total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol; triglycerides; apolipoprotein B; insulin; glucose; and antioxidants at week 12 of each treatment period, compared among the 4 groups.

RESULTS: Dietary treatment decreased levels of total cholesterol by 7.6% (P<.001), LDL cholesterol by 10.8% (P<.001), HDL cholesterol by 4.9% (P =.01), apolipoprotein B by 5.7% (P =.003), serum insulin by 14.0% (P =.02), and alpha-tocopherol by 3.5% (P =.04). Simvastatin decreased levels of total cholesterol by 20.8%, LDL cholesterol by 29.7%, triglycerides by 13.6%, apolipoprotein B by 22.4%, alpha-tocopherol by 16.2%, beta-carotene by 19.5%, and ubiquinol-10 by 22.0% (P<.001 for all) and increased levels of HDL cholesterol by 7.0% (P<.001) and serum insulin by 13.2% (P =.005). Glucose levels remained unchanged in all groups. The effects of dietary treatment and simvastatin were independent and additive.

CONCLUSIONS: A modified Mediterranean-type diet rich in omega-3 fatty acids efficiently potentiated the cholesterol-lowering effect of simvastatin, counteracted the fasting insulin-elevating effect of simvastatin, and, unlike simvastatin, did not decrease serum levels of beta-carotene and ubiquinol-10.

Oxidized low-density lipoproteins (ox-LDLs) appear to play a significant role in atherogenesis. In fact, circulating ox-LDL concentrations have been recognized as a risk factor for cardiovascular disease (CVD). A higher intake of some nutrients and specific food compounds such as monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs) and flavonoids have also been associated with a lower risk of CVD. These dietary factors could be associated to a lower risk of CVD through a reduction of the atherogenicity of LDL particles through limited oxidation. Therefore, the purpose of this article is to review human clinical studies that evaluated effects of dietary antioxidant vitamins, fatty acids (MUFA, PUFA) and specific flavonoid-rich foods on LDL particle oxidation and describe potential mechanisms by which dietary factors may prevent oxidation of LDL particles. Antioxidant vitamin supplements such as alpha-tocopherol and ascorbic acid as well as beta-carotene and fish-oil supplements have not been clearly demonstrated to prevent oxidation of LDL particles. Moreover, inconsistent documented effects of flavonoid-rich food such as olive oil, tea, red wine and soy on LDL particle oxidizability may be explained by difference in variety and quantity of flavonoid compounds used among studies. However, a healthy food pattern such as the Mediterranean diet, which includes a combination of antioxidant compounds and flavonoid-rich foods, appears effective to decrease LDL particle oxidizability, which may give some insight of the cardiovascular benefits associated with the Mediterranean diet.

In the present study, we investigated the effects of histidine and vitamin C (alone or in combination) treatments against isoproterenol (aβ-adrenergic receptor agonist)-induced acute myocardial infarction in rats. We used propranolol (a β-adrenergic receptor blocker) to compare the results. Rats were given intraperitoneal injections of histidine (40 mg kg(-1)) and vitamin C (40 mg kg(-1)) alone and combined daily for 21 days. Propranolol (10 mg kg(-1)) was orally administered daily for 10 days (from day 11 to day 21). Myocardial infarction was induced by subcutaneous injections of 150 mg kg(-1) of isoproterenol at an interval of 24 hr on days 20 and 21. Blood and tissue samples were taken for histopathological and biochemicalevaluations following electrocardiography recording on day 21. Isoproterenol elevated ST segment, increased heart weight, heart rate, serum activities of aspartate transaminase, lactate dehydrogenase, creatine kinase-MB and heart tissue content of malondialdehyde, and decreased R wave amplitude andsuperoxide dismutase and catalase activities of heart tissue. Necrosis, edema and inflammatory cells infiltration were observed in myocardial tissue sections. Our results indicated that histidine and vitamin C alone, and especially in combination prevent isoproterenol-induced cardiotoxicity and havesimilar protective effects with propranolol. Cardioprotective effects of histidine and vitamin C may be associated with their ability to reduce free radical-induced toxic effects.

The biochemical mechanisms by which hypertension accelerates atherosclerosis and increases the risk of aortic aneurysm rupture are poorly understood. This study evaluates the effects of hypertension on aortic trace element concentrations and antioxidant status in tissue removed from 26 normotensive (NT) and 20 hypertensive (HT) patients. Twenty-seven of 46 patients (59%) had aneurysmal (AA), and 19 of 46 (41%) had occlusive disease (OD). Aortic iron concentrations were markedly higher in both OD and AA tissue compared with controls. A similar trend was observed with copper concentrations, with the highest elevations observed in HT AA tissues. No significant differences were observed in zinc concentrations, except that HT AA aorta had significantly lower zinc levels than either OD or control tissue. Aortic ascorbic acid concentrations in diseased aorta were lower than those of controls, but independent of blood pressure. Copper-zinc-superoxide dismutase activity was similarly reduced, with the lowest activity observed in diseased aorta from HT patients. Only HT AA aorta had significantly higher manganese-superoxide dismutase activity than controls. The aortas of patients with AA had significantly lower amounts of elastin and greater elastase activity than either controls or those with OD. However, the differences were independent of blood pressure. Hypertensive patients with OD and AA had 31% more and 27% less aortic collagen, respectively, than their NT counterparts (P less than 0.05). These data suggest that the reduction in aortic collagen and elastin in HT patients with AA compared with their NT counterparts may explain the larger size of aneurysms and predispose to their eventual rupture. Furthermore, the diminished antioxidant status associated with HT predisposes to lipid peroxidation, which contributes to the acceleration of these processes. Our studies were conducted in patients with established aortic aneurysmal and occlusive disease. Whether these observations are pertinent to the pathogenesis of AA and OD remains unclear and merits further study.

BACKGROUND:The purpose of this study is to determine the effect of L-ascorbic acid and alpha-tocopherol as well as combination of these vitamins with or without exposure to physical exercise on intensity of lipid peroxidation, activity of xanthine oxidase, activity of total antioxidative system, concentration of glutathione, and activity of catalase in the serum of guinea pigs.

MATERIALS AND METHODS:The experimental measurements of intensity of lipid peroxidation, activity of xanthine oxidase, activity of total antioxidative system, concentration of glutathione, and activity of catalase were done in the serum of guinea pigs. The animals were exposed to the test load to achieve exhaustion and the test was terminated when the animal for the third time to sink into the water.

RESULTS:The results of this study demonstrated that endurance exercise of guinea pigs induced oxidative stress response in terms of increased lipid peroxidation and activity of xanthine oxidase in the serum of experimental animals. Our study investigated the antioxidant activity of L-ascorbic acid and alpha-tocopherol also measuring three protective markers in the serum: total antioxidant activity, content of glutathione and activity of catalase. The results obtained show that the vitamins influence the concentrations of above mentioned biochemical parameters, which points out their protective effect of swimming-induced oxidative stress.

CONCLUSION:Single or combined administration of L-ascorbic acid and alpha-tocopherol caused significant inhibition of these markers indicating the important antioxidant activity of the vitamins. Results lead to conclude that the combined treatments with vitamins with or without exposure to physical exercise showed the clear synergistic effect..

BACKGROUND:The purpose of this study is to determine the effect of L-ascorbic acid and alpha-tocopherol as well as combination of these vitamins with or without exposure to physical exercise on intensity of lipid peroxidation, activity of xanthine oxidase, activity of total antioxidative system, concentration of glutathione, and activity of catalase in the serum of guinea pigs.

MATERIALS AND METHODS:The experimental measurements of intensity of lipid peroxidation, activity of xanthine oxidase, activity of total antioxidative system, concentration of glutathione, and activity of catalase were done in the serum of guinea pigs. The animals were exposed to the test load to achieve exhaustion and the test was terminated when the animal for the third time to sink into the water.

RESULTS:The results of this study demonstrated that endurance exercise of guinea pigs induced oxidative stress response in terms of increased lipid peroxidation and activity of xanthine oxidase in the serum of experimental animals. Our study investigated the antioxidant activity of L-ascorbic acid and alpha-tocopherol also measuring three protective markers in the serum: total antioxidant activity, content of glutathione and activity of catalase. The results obtained show that the vitamins influence the concentrations of above mentioned biochemical parameters, which points out their protective effect of swimming-induced oxidative stress.

CONCLUSION:Single or combined administration of L-ascorbic acid and alpha-tocopherol caused significant inhibition of these markers indicating the important antioxidant activity of the vitamins. Results lead to conclude that the combined treatments with vitamins with or without exposure to physical exercise showed the clear synergistic effect..