Plasma Lipid Peroxide Levels Research Articles

Anti-Stress Effect of Oolong Tea in Women Loaded with Vigil

The preventive effect of oolong tea on vigil stress was investigated in 55 Chinese women. The subjects received 4 servings of tea bag daily, the tea bags in each containing 2 g dry weight of oolong tea or barley tea, or else water, for a period of one week. The results of a questionnaire indicated that ingestion of oolong tea improved symptoms of stress such as stiffness of the shoulders, fatigue of the eyes and headaches, as well as ameliorated the stress-induced increase in the number of errors in calculation tasks compared with controls. In addition, plasma cortisol levels were significantly lower in the oolong tea group (17.84 ± 2.46 µg/dl) than in the barley tea group (21.33 ± 6.47 µg /dl) or water group (22.95 ± 6.98 µg/dl). Ingestion of oolong tea significantly alleviated the vigil stress-induced increase in plasma lipid peroxide levels, which may have been related to the stress-relieving effects of caffeine or antioxidant properties of polyphenols contained in the tea. These findings suggested that oolong tea has anti-stress effect, with no adverse effects on appetite or physical fitness.

Effects of Certain Micronutrients and Melatonin on Plasma Lipid, Lipid Peroxidation, and Homocysteine Levels in Rats

Background Numerous studies suggest an association between high intake of antioxidant vitamins and fish oil and reduced risk of coronary heart disease. Hyperhomocysteinemia has also been identified as an independent risk factor for arteriosclerosis. In this paper, we aimed to evaluate the effects of vitamin E, vitamin C, vitamin C 6 palmitate (VC6P), lipoic acid, fish oil, and melatonin supplementation on lipid peroxidation, plasma lipid, and homocysteine (Hcy) levels in rats. Methods Animals were divided into seven groups: one was used as control and each remaining group was supplemented with one substance for 6 weeks. All substances were dissolved in olive oil and injected intraperitoneally (i.p.) with the exception of vitamin C, which was dissolved in drinking water. Plasma Hcy, lipid peroxidation, and lipids were determined. Results Plasma malondialdehyde (MDA) levels decreased significantly in melatonin ( p <0.01), lipoic acid ( p <0.01), and vitamin E ( p <0.05) groups. On the other hand, supplementation with vitamin C and VC6OP lowered MDA levels moderately but not significantly ( p >0.05). Fish oil supplementation caused a slight but insignificant increase in plasma MDA levels ( p >0.05). Plasma lipid levels in animals treated with melatonin, vitamin E, vitamin C, lipoic acid, and fish oil were significantly lower than those of controls; however, treatment of rats with VC6P has no significant effect on plasma lipid level. Melatonin and fish oil administration significantly lowered plasma Hcy levels, whereas VC6P elevated its level. There was no significant effect of vitamin E, vitamin C, and lipoic acid on levels of plasma Hcy. Conclusions Our data suggest that supplementation with antioxidants appears to be hypolipidemic. In addition to these beneficial effects, administration of melatonin and fish oil deserves careful consideration as a measure to lower plasma Hcy levels and reduce risk of cardiovascular diseases.

Vitamin C and E supplements improve the impaired antioxidant status and decrease plasma lipid peroxides in hemodialysis patients☆

This study investigated the supplementation with vitamin C or/and E on the antioxidant system in hemodialysis patients. Thirty-eight hemodialysis patients (27 males and 11 females) with the average of 60 years old were divided into four groups: placebo (400 mg starch/time), vitamin C (400 mg/time)-, vitamin E (400 mg d,l- α-tocopheryl acetate/time)-, and vitamin C (400 mg/time) + E (400 mg d,l- α-tocopheryl acetate/time)-supplemented groups for 6-week supplementation. The patients orally received three capsules of placebo or antioxidant(s) three times a week after finishing hemodialysis. Thirty-six healthy subjects (22 males and 14 females) with the average of 58 years old were recruited as the control group. Hemodialysis patients significantly decreased plasma vitamin C by 32%, erythrocyte glutathione by 26%, and plasma total antioxidant status by 9%, but increased plasma lipid peroxide levels by 102% compared with the control group at the baseline. The levels of plasma vitamin C and total antioxidant status significantly decreased by 24% and 18%, respectively, from the post-dialysate compared with those from the pre-dialysate. At week 6, vitamin C + E-supplemented group significantly increased plasma vitamin C and E, erythrocyte glutathione, and plasma antioxidant status, and inhibited plasma lipid peroxides compared with placebo group. Additionally, vitamin C + E-supplemented group had higher plasma vitamin C, vitamin E, and total antioxidant status, and lower plasma lipid peroxides than placebo group even at least 2 weeks after the termination of the supplements. Therefore, antioxidant vitamin supplements could improve antioxidant status and decrease lipid peroxides of hemodialysis patients.

In vivo treatment with stobadine prevents lipid peroxidation, protein glycation and calcium overload but does not ameliorate Ca 2+-ATPase activity in heart and liver of streptozotocin-diabetic rats: comparison with vitamin E

Hyperglycemia leads to excess production of reactive oxygen species (ROS), lipid peroxidation and protein glycation that may impair cellular calcium homeostasis and results in calcium sequestration and dysfunction in diabetic tissues. Stobadine (ST) is a pyridoindole antioxidant has been postulated as a new cardio- and neuroprotectant. This study was undertaken to test the hypothesis that the treatment with ST inhibits calcium accumulation, reduces lipid peroxidation and protein glycation and can change Ca 2+,Mg 2+-ATPase activity in diabetic animals. The effects of vitamin E treatment were also evaluated and compared with the effects of combined treatment with ST. Diabetes was induced by streptozotocin (STZ, 55 mg/kg i.p.). Some of diabetic rats and their age-matched controls were treated orally with a low dose of ST (24.7 mg/kg/day), vitamin E (400–500 IU/kg/day) or ST plus vitamin E for 10 weeks. ST and vitamin E separately produced, in a similar degree, reduction in diabetes-induced hyperglycemia. Each antioxidant alone significantly lowered the levels of plasma lipid peroxidation, cardiac and hepatic protein glycation in diabetic rats but vitamin E treatment was found to be more effective than ST treatment alone. Diabetes-induced increase in plasma triacylglycerol levels was not significantly altered by vitamin E treatment but markedly reduced by ST alone. The treatment with each antioxidant completely prevented calcium accumulation in diabetic heart and liver. Microsomal Ca 2+,Mg 2+-ATPase activity significantly decreased in both tissues of untreated diabetic rats. ST alone significantly increased microsomal Ca 2+,Mg 2+-ATPase activity in the heart of normal rats. However, neither treatment with ST nor vitamin E alone, nor their combination did change cardiac Ca 2+,Mg 2+-ATPase activity in diabetic heart. In normal rats, neither antioxidant had a significant effect on hepatic Ca 2+,Mg 2+-ATPase activity. Hepatic Ca 2+,Mg 2+-ATPase activity of diabetic rats was not changed by single treatment with ST, while vitamin E alone completely prevented diabetes-induced inhibition in microsomal Ca 2+,Mg 2+-ATPase activity in liver. Combined treatment with ST and vitamin E provided more benefits in the reduction of hyperglycemia and lipid peroxidation in diabetic animals. This study describes potential mechanisms on cellular effects of ST in the presence of diabetes-induced hyperglycemia that may delay or inhibit the development of diabetic complications. The use of ST together with vitamin E can better control hyperglycemia-induced oxidative stress.

Relationship between physical activity and oxidative stress biomarkers in women

To examine the relationship between physical activity and levels of plasma lipid peroxides, superoxide dismutase in erythrocytes (SOD), and glutathione peroxidase (GSH-Px) in whole blood activities. Cross-sectional study in 488 Spanish women. Two categories of leisure time physical activity were defined according to their intensity: low (<or=6 METs) and high (>6 METs). Energy expenditure in household activities was also recorded. Multivariate linear regression analyses were used to adjust for the effect of physical activity on lipid peroxides and SOD and GSH-Px for confounding variables. The amount of leisure time physical activity was associated with high activity levels of SOD (P = 0.022) and GSH-Px (P = 0.002). Similar results were obtained when physical activity in household activities was added to total leisure physical activity. Physical activity of low intensity was associated with high SOD activity levels (P = 0.002) and that of high intensity with high GSH-Px activity levels (P = 0.001). The amount and intensity of leisure physical activity were directly related to both antioxidant enzyme activity levels. The findings of this study suggest a modulatory effect of leisure physical activity intensity on antioxidative balance in the studied female population.

Elevated plasma lipid peroxide levels in angina pectoris and myocardial infarction

Background: The concept that oxidised low-density lipoprotein (LDL), not native LDL, plays a major role in atherogenesis is gaining support. Lipid hydroperoxides in plasma are carried almost exclusively in LDL and reflect oxidised LDL. Previously, elevated plasma lipid hydroperoxides were reported in coronary artery disease (CAD) patients following bypass surgery. To determine whether the increased lipid hydroperoxide was related to bypass or reflected ongoing atherosclerosis, plasma lipid hydroperoxide was measured in acute myocardial infarction (AMI) and stable angina. Methods: Patients with AMI ( n=39) and stable angina ( n=40) were compared with matched controls. Lipids and lipoproteins were selectively removed from plasma by absorption to Liposorb gel. Lipid hydroperoxide concentration in the gel was measured by a sensitive triiodide spectrophotometric technique. Results: Lipid hydroperoxide levels in AMI and stable angina were elevated (3.47±0.21 μmol/l, P<.001 and 3.76±0.24 μmol/l, P<.001) compared to controls (2.18±0.13 μmol/l). Previously, a concentration >3 μmol/l was considered pathological. Using this criterion, we detected pathological lipid hydroperoxide concentrations in 10.3% of controls, 57.5% of AMI and 61.5% of angina patients. Conclusion: Plasma lipid hydroperoxide levels are significantly elevated in AMI and angina. This is not attributable to previous cardiopulmonary bypass but to the presence of atherosclerotic disease and is likely to play a role in atherogenesis.

A lipoprotein lipase activator, NO-1886 prevents impaired endothelium-dependent relaxation of aorta caused by exercise in aged rats

Exercise decreases plasma total cholesterol and triglycerides, and simultaneously, increases high density lipoprotein (HDL) cholesterol. As a result, exercise is believed to aid in preventing atherosclerosis. However, we do not know whether exercise protects against the development of atherosclerosis in the elderly. The aim of this study was to ascertain whether the lipoprotein lipase activator NO-1886 had an effect on the prevention of atherosclerosis in aged rats which undergo exercise. Exercise for 3 months did not affect plasma lipids but decreased the accumulation of visceral fat in 2-year-old rats (aged rat). Exercise also resulted in an elevation of plasma lipid peroxide (LPO) levels and impaired the endothelium-dependent relaxation of the thoracic aorta caused by acetylcholine in aged rats. On the other hand, NO-1886 decreased plasma triglycerides and increased HDL cholesterol and suppressed the elevation of plasma LPO levels caused by exercise. Furthermore, NO-1886 prevented impaired endothelium-dependent relaxation caused by exercise. In summary, the results of our study indicate that exercise may cause impaired endothelium-dependent relaxation by elevation of LPO in aged rats, and that NO-1886 prevents this impaired endothelium-dependent relaxation of aorta by reducing plasma triglycerides, elevating HDL cholesterol, and suppressing the elevation of plasma LPO caused by exercise.

Determination of serum aluminum, platelet aggregation and lipid peroxidation in hemodialyzed patients.

Aluminum (Al3+) overload is frequently associated with lipid peroxidation and neurological disorders. Aluminum accumulation is also reported to be related to renal impairment, anemia and other clinical complications in hemodialysis patients. The aim of the present study was to determine the degree of lipid peroxidation, platelet aggregation and serum aluminum in patients receiving regular hemodialytic treatment. The level of plasma lipid peroxidation was evaluated on the basis of thiobarbituric acid reactive substances (TBARS). Mean platelet peroxidation in patients undergoing hemodialysis was significantly higher than in normal controls (2.7 +/- 0.03 vs. 1.8 +/- 0.06 nmol/l, P<0.05). Platelet aggregation and serum aluminum levels were determined by a turbidimetric method and atomic absorption spectrophotometry, respectively. Serum aluminum was significantly higher in patients than in normal controls (44.5 +/- 29 vs. 10.8 +/- 2.5 microg/l, P<0.05). Human blood platelets were stimulated with collagen (2.2 microg/ml), adenosine diphosphate (6 microM) and epinephrine (6 microM) and showed reduced function with the three agonists utilized. No correlation between aluminum levels and platelet aggregation or between aluminum and peroxidation was observed in hemodialyzed patients.

Effects of Octreotide on Lipid Peroxidation in Pancreas and Plasma in Acute Hemorrhagic Necrotizing Pancreatitis in Rats

Background: The therapeutic effects of octreotide in acute hemorrhagic necrotizing pancreatitis (ANP) have always been considered to be due to the inhibition of the exocrine pancreatic secretion in order to reduce pancreatic autodigestion. In this experimental study we analyzed whether octreotide has also antioxidative effects on acute pancreatitis. Methods: 40 male Wistar rats were randomized into four groups (n = 10). Group 1 underwent a laparotomy. Groups 2–4 received an injection of natrium taurocholate into the pancreatic duct to induce acute pancreatitis. One hour later group 2 was injected 1 ml NaCl solution intraperitoneally, while groups 3 and 4 received 0.1 or 0.2 mg octreotide, respectively. The severity of ANP was examined histologically. The lipid peroxide level as well as the activity of glutathione peroxidase and superoxide dismutase were measured in plasma and pancreatic tissue samples. Results: High-dose octreotide decreased the lipid peroxide level in plasma (2.1 ± 0.53 vs. 4.69 ± 1.35 nmol/l; p < 0.05) and pancreatic tissue samples 4.67 ± 1.37 vs. 13.20 ± 2.93 nmol/ml; p < 0.05) compared to the pancreatitis control group. Low-dose octreotide, however, did not reduce lipid peroxidation. Conclusion: Octreotide seems to have a dose-dependent antioxidative effect in natrium taurocholate-induced pancreatitis in rats.

Effects of Added Dietary Taurine on Erythrocyte Lipids and Oxidative Stress in Rabbits Fed a High Cholesterol Diet

Lipid peroxidation leads to damage of polyunsaturated fatty acids of membrane phospholipids. The contribution of oxidative stress to hypercholesterolemia-induced hemolytic anemia and the effects of addition of taurine on erythrocyte lipid composition, oxidative stress, and hematological data were studied in rabbits fed on a high cholesterol (HC) diet (1%, w/w) for 2 months. The effects of taurine on erythrocyte hemolysis and H2O2-induced lipid peroxidation were investigated in normal rabbit erythrocytes in vitro. The HC diet resulted in increases in plasma lipids and lipid peroxide levels as well as increases in cholesterol levels and the cholesterol:phospholipid ratio in the erythrocytes. This diet caused a hemolytic anemia, but lipid peroxide levels remained unchanged in the erythrocytes of the rabbits. Taurine (2.5%, w/w) added to the food has an ameliorating effect on plasma lipids and lipid peroxide levels in rabbits fed on a HC diet. This treatment also caused decreases in elevated erythrocyte cholesterol levels and cholesterol:phospholipid ratio due to the HC diet, but it did not prevent the hemolytic anemia and did not change erythrocyte lipid peroxide levels. In addition, in an in vitro study, taurine did not protect erythrocytes against H2O2-induced hemolysis or lipid peroxidation. These results show that the HC diet causes hemolytic anemia without any changes in erythrocyte lipid peroxidation, and taurine treatment was not effective against hemolytic anemia caused by the HC diet.

Protective effect of green tea extract against the erythrocytic oxidative stress injury during mycobacterium tuberculosis infection in mice.

The present study has been undertaken to monitor the extent of oxidative stress in mice infected with M tuberculosis and the role of crude green tea extract in repairing the oxidative damage. The mice were divided into three groups of 9 each; normal, infected-untreated and infected-treated. The infected group of animals exhibited significant enhancement of erythrocytic catalase and glutathione peroxidase activities along with elevated levels of erythrocytic total thiols and plasma lipid peroxidation as compared to normal animals. The infected group also exhibited significantly decreased activity of superoxide dismutase and levels of glutathione in erythrocytes. Upon oral administration of green tea extract for seven days the oxidative stress parameters were reverted back to near normal levels as evidenced by a fall in catalase, glutathione peroxidase, total thiol and extent of lipid peroxidation with concomitant increase in the levels of SOD and reduced glutathione in infected animals. The findings thus, portray that there is a high oxidative stress during early stages of tuberculosis and antioxidants such as green tea extract, can play a vital role by reducing stress through adjuvant therapy.

Fluvastatin reduces modification of low-density lipoprotein in hyperlipidemic rabbit loaded with oxidative stress

The in vivo antioxidant effect of fluvastain, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, was investigated using Watanabe heritable hyperlipidemic (WHHL) rabbits subjected to nicotine-free cigarette smoke extracts as oxidative stress. Fluvastatin was given orally at doses of 10 and 30 mg/kg per day for 5 months. The cigarette smoke extracts were prepared by bubbling the gas phase of smoke into phosphate-buffered saline and was injected daily into the rabbit ear vein. The rabbits chronically treated with the cigarette smoke extracts showed an increase in plasma lipid peroxide levels, estimated as thiobarbituric acid-reactive substances. Oxidative modification of plasma low-density lipoprotein (LDL) was assessed by anion-exchange high-performance liquid chromatographic analysis, LDL susceptibility to oxidation, LDL incorporation into macrophages and thiobarbituric acid-reactive substances levels in LDL. Treatment with fluvastatin significantly reduced these effects induced by the cigarette smoke extracts in a dose-related manner and exerted a cholesterol-lowering effect. At the end of the experiment, the cigarette smoke extracts caused accumulation of cholesteryl ester in the thoracic aorta, while fluvastatin significantly prevented this accumulation. These results indicate that fluvastatin can exert an antioxidant effect in vivo, with a strong effect on oxidative stress such as smoking, a major risk factor of atherosclerosis.

Immune response to Newcastle disease virus in broilers: a useful model for the assessment of detoxification of ervil seeds

Ervil (Vicia ervilia) seeds are produced in the Mediterranean region and used as a source of protein for cattle and poultry. The methods used to assess the toxic effects of legume seeds in the feed of poultry include the observation of one or more parameters, including abnormal signs, weight gain, feed consumption, gall bladder weight, pancreas weight, pancreas proteolytic and amylase activity, haemolysis of red blood cells, liver weight, liver glutathione level, liver and plasma lipid levels, and plasma lipid peroxide levels. The authors describe the use of quantitative determination of the immune response to Newcastle disease virus (NDV) vaccine in broilers as a model that can be used to assess different detoxification treatments of ervil seeds. Broiler chicks fed differently-treated ervil, supplemented as 25% of the diet, at one to four weeks of age and vaccinated intraocularly with live NDV vaccine at eight days of age, showed different immune responses at three weeks post vaccination. Immunosuppression with regards to NDV was apparent in the group of birds raised on untreated ervil supplement, resulting in a mean immune response (titre) of 798.5. Five of the six different treatments of ervil seeds resulted in different degrees of rectification of the immunosuppression, with some broilers reaching a mean NDV immune titre of 2070.6, similar to that obtained in control broilers raised on a basal diet with no ervil seed supplement (mean NDV immune titre of 2333.8; P > 0.05). The five successful treatments of ervil (in increasing order of rectification of immunosuppression in broilers, with mean NDV titres in parentheses) were: ground soaked dried ervil (971.6), ground autoclaved dried ervil (1223.1), soaked autoclaved dried ervil (1273.1), soaked dried ervil (1340.0), and ground-soaked autoclaved dried ervil (2070.6).

Effect of yiqitongyanghuatan recipe on experimental atherosclerosis in rabbits.

In order to investigate the roles of Yiqitongyanghuatan (YQTYHT) recipe in reducing the levels of serum cholesterol and plasma lipid peroxidation (LPO), platelet aggregation function (PAgF) and platelet adhesion function (PAdF), the area of atherosclerotic plague coverage in aorta and the thickness of plague, 32 male Japanese white rabbits were divided into 4 groups. The results showed that the YQTYHT recipe could significantly lower the levels of serum cholesterol and tryglyceride, plasma LPO, and PAgF and PadF. The area of atherosclerotic plague coverage in aorta and the thickness of plague in the YQTYHT-fed rabbits were decreased as compared with that in the high-cholesterol-fed rabbits. The above roles might contribute to the main mechanism of YQTYHT against atherosclerosis.

Reduced erythrocyte membrane essential fatty acids and increased lipid peroxides in schizophrenia at the never-medicated first-episode of psychosis and after years of treatment with antipsychotics

Abnormal membrane phospholipid essential polyunsaturated fatty acid (EPUFA) metabolism (i.e., reduced incorporation into phospholipids and increased breakdown) has been suggested to contribute to the etiopathophysiology of schizophrenia. However, most of the published studies have reported changes in the levels of membrane EPUFA in chronic medicated patients or in drug-naive patients long after onset of illness (1–2 years). Since the EPUFA metabolism can be altered by years of untreated illness or differentially altered by various antipsychotics, the significance of EPUFA membrane status to schizophrenia psychopathophysiology is unclear. We report the erythrocyte membrane EPUFA levels in drug-naive patients within ±4.5 days of onset of psychosis from an Army Medical Center, and in patients treated years with antipsychotics from a Veterans Affairs Medical Center. The levels of plasma lipid peroxides (TBARS, thiobarbituric acid reactive substances), products of damaged EPUFAs, were also determined. The levels of EPUFAs, particularly arachidonic acid (AA) and docosahexaenoic acid (DHA) were significantly lower ( P<0.001) in drug-naive patients at the onset of psychosis compared to matched normal controls. These lower EPUFA levels were associated with significantly higher levels of TBARS in patients ( P<0.001). The levels of AA and DHA were also lower ( P<0.001) and TBARS higher in chronic medicated patients than normal controls. However, the EPUFA levels were higher in chronic medicated patients than drug-naive first-episode patients. These data indicate that lower membrane AA and DHA most likely predate the illness and probably contribute to the onset of illness, and furthermore treatment with some antipsychotics may increase the levels of EPUFAs. The lipid peroxidation data suggest that possible increased oxidative stress, either as a part of the illness and/or its treatment with antipsychotics, may be one of the mechanisms of reduced membrane EPUFAs. These findings may have a significant impact on improving strategies for supplementation of EPUFAs and antioxidants to improve the outcome of schizophrenia.

Antioxidative activity of naringin and lovastatin in high cholesterol-fed rabbits

The consumption of a cholesterol-enriched diet increases the degree of lipid peroxidation, which is one of the early processes of atherosclerosis. The aim of this trial was to determine the antioxidative effects of the citrus bioflavonoid, naringin, a potent cholesterol-lowering agent, compared to the cholesterol-lowering drug, lovastatin, in rabbits fed a high cholesterol diet. Male rabbits were served a high-cholesterol (0.5%, w/w) diet or high-cholesterol diet supplemented with either naringin (0.5% cholesterol, 0.05% naringin, w/w) or lovastatin (0.5% cholesterol, 0.03% lovastatin, w/w) for 8 weeks to determine the plasma and hepatic lipid peroxide, plasma vitamin A and E levels, and hepatic hydrogen peroxide levels, along with the hepatic antioxidant enzyme activities and gene expressions. Only the lovastatin group showed significantly lower plasma and hepatic lipid peroxide levels compared to the control group. The naringin supplementation significantly increased the activities of both hepatic SOD and catalase by 33% and 20%, respectively, whereas the lovastatin supplementation only increased the catalase activity by 23% compared to control group. There was no difference in the GSH-Px activities between the various groups. Content of H 2O 2 in hepatic mitochondria was significantly lower in groups supplemented with lovastatin and naringin than in control group. However, there was no difference in cytosolic H 2O 2 content in liver between groups. The concentration of plasma vitamin E was significantly increased by the naringin supplementation. When comparing the antioxidant enzyme gene expression, the mRNA expression of SOD, catalase and GSH-Px was significantly up-regulated in the naringin-supplemented group. Accordingly, these results would appear to indicate that naringin, a citrus bioflavonoid, plays an important role in regulating antioxidative capacities by increasing the SOD and catalase activities, up-regulating the gene expressions of SOD, catalase, and GSH-Px, and protecting the plasma vitamin E. In contrast, lovastatin exhibited an inhibitory effect on the plasma and hepatic lipid peroxidation and increased the hepatic catalase activity in high-cholesterol fed rabbits.

Heme oxygenase-1 inhibits atherogenesis in Watanabe heritable hyperlipidemic rabbits.

Heme oxygenase-1 (HO-1) is proposed to have a variety of adaptive responses against oxidative stress. To examine the function of HO-1 against atherogenesis in vivo, we observed the effects of HO-1 inhibition on atherosclerotic lesion formation in Watanabe heritable hyperlipidemic rabbits (WHHL). Methods and Results- During 4 weeks of a 1% cholesterol diet, intravenous injections of Sn-protoporphyrin IX to inhibit HO-1 (S group, n=10) and saline as a control (C group, n=10) were given to 3-month-old WHHL rabbits. The percentages of en face atherosclerotic lesion areas in total descending aorta by Sudan IV staining (EFA) and the ratio of intima to media in microscopic atherosclerotic lesions in the ascending aortas (I/M) were calculated. Two different quantitative methods revealed significantly greater atherosclerotic lesions in the S group than the C group (EFA, P<0.001; I/M, P<0.005). HO-1 expression in atherosclerotic lesions was confirmed by Northern blot and immunohistochemical analyses. The dominant cell types expressing HO-1 were macrophages and foam cells, in which oxidized phospholipids were also accumulated. HO inhibition increased plasma and tissue lipid peroxide levels without affecting plasma lipid co osition. These results suggest the possibilities that HO-1 has antiatherogenic properties in vivo and that the antiatherogenic properties of HO-1 are conducted through the prevention of lipid peroxidation.

Effects of Dietary Fat and Endurance Exercise on Plasma Cortisol, Prostaglandin E2, Interferon-γ and Lipid Peroxides in Runners

Objective: Exercise and the neuroendocrine and oxidative stress it elicits on immune function is modulated by dietary fat intake. The effects of increasing dietary fat on endurance exercise-induced alterations (80% of V̇O2max for 2 hours) in the plasma levels of cortisol and prostaglandin E2 (PGE2), interferon-γ (IFN-γ) and lipid peroxides were investigated. As higher levels of cortisol, PGE2 and lipid peroxides could be immunosuppressive, the effects of different levels of dietary fat on these measures in runners were determined.Methods: Healthy trained runners (males and females) consumed serially 15% fat diet (of daily energy), 30% fat diet and 40% fat diets for four weeks each. In the last week of each diet period the subjects ran to exhaustion at 80% of their V̇O2max and blood was drawn pre- and post-run. Cortisol, IFN-γ, PGE2 and lipid peroxides were determined using standard techniques.Results: Pre-exercise levels of plasma cortisol were elevated, IFN-γ was unchanged and PGE2 and lipid peroxides decreased on the 40%F diet compared to 30%F and 15%F. Post-exercise levels of plasma cortisol (p < 0.004), PGE2 (p < 0.0057) and lipid peroxide levels increased (p < 0.0001) after endurance exercise on all diets. The rates of increase of plasma cortisol levels during exercise were similar on all three diets. Although absolute cortisol levels were higher in the high fat group, the rate of increase of plasma cortisol level during exercise was similar on each diet. The dietary fat levels did not affect IFN-γ, however, PGE2 and lipid peroxides decreased with increasing fat at baseline at 40%F level (p < 0.01; 30%F vs. 40%F: p < 0.002; 15%F vs. 40%F: p < 0.007).Conclusions: Data from the present study suggest that higher levels of fat in the diet, up to 40%, increase endurance running time without adverse effects on plasma cortisol, IFN-γ, and lipid peroxide levels.

Effects of fish oil and vitamin E on the antioxidant defense system in diet-induced hypercholesterolemic rabbits

This study was designed to investigate the effects of fish oil and vitamin E on the antioxidant defense system in hypercholesterolemic rabbits. A high fat and cholesterol diet, with or without supplement by fish oil and/or a vitamin E supplement, was fed to rabbits for 6 weeks. Compared to the reference diet of regular laboratory rabbit chow, a high fat and cholesterol-enriched diet increased atheroma formation, plasma lipid and peroxide levels, decreased blood glutathione levels, and reduced plasma glutathione reductase, glutathione peroxidase, and catalase activities. Fish oil supplementation significantly reduced atheroma and increased glutathione reductase and glutathione peroxidase activities and blood glutathione levels, but increased plasma lipid peroxide levels. Vitamin E supplementation of the fish oil diet enhanced the beneficial effects by increasing glutathione reductase activity and decreasing peroxide levels. These results indicate that a high fat and cholesterol diet attenuates blood glutathione levels and plasma antioxidant enzyme activities, which may account for some of its atherogenic properties. Consumption of fish oil enhances antioxidative defenses against the oxidative stress imposed by hypercholesterolemia, and vitamin E further enhances these beneficial effects.

Effects of aminoguanidine and desferrioxamine on some vascular and biochemical changes associated with streptozotocin-induced hyperglycaemia in rats

The effects of aminoguanidine (AG; 100 mgkg−1) and desferrioxamine (DFO; 50 mgkg−1) on some vascular and biochemical changes associated with streptozotocin (STZ; 65 mgkg−1; i.p.)-induced hyperglycaemia were investigated in rats. Both AG and DFO were administered i.p., once daily, for 14 consecutive days to normal and hyperglycaemic animals. The responsiveness of the isolated aortic rings to phenylephrine (PE) was tested. In addition, biochemical markers for oxidative stress such as plasma levels of lipid peroxides and total thiols, as well as the activities of erythrocytic superoxide dismutase (SOD) and whole blood glutathione peroxidase (GSH-Px) were assessed. Results of the present study indicated that induction of hyperglycaemia was associated with increased aortic ring responsiveness to PE, loss in body weight, increase in urine volume, elevation of plasma total thiols and lipid peroxide levels and elevated SOD and GSH-Px enzymatic activities. Treatment of normal rats with AG reduced the response of their aortae to PE. Furthermore, a profound increase in body weight without any significant change in the measured biochemical parameters was observed. In hyperglycaemic animals, AG tended to normalize the enhanced aortic response to PE and modulated STZ-induced biochemical changes without affecting the elevated plasma glucose level. Treatment of normal rats with DFO reduced the response of their aortae to PE and decreased their body weight without altering any of the chosen biochemical parameters. In hyperglycaemic animals, DFO attenuated the responsiveness of their aortae to PE and at the same time, did not affect the loss in body weight and the elevation of plasma glucose level observed in the hyperglycaemic group. Additionally, DFO normalized the elevated plasma level of total thiols and exerted a modulatory influence on the enhanced activities of SOD and GSH-Px as well as on the increased levels of lipid peroxides. Our data lend further credence for the contribution of oxidative stress in the vascular and biochemical changes associated with STZ-induced hyperglycaemia. It is also apparent that advanced glycosylation end products and nitric oxide might be involved. Until clinical studies prove the efficacy and safety of these drugs, specific agents which could scavenge free radicals and block protein glycosylation seem beneficial as a helpful adjunct to the therapy of diabetes.