Increased Serum Lipid Peroxidation Research Articles

Evaluation of Vitamin D, Vitamin D Binding Protein Gene Polymorphism with Oxidant - Antioxidant Profiles in Chronic Obstructive Pulmonary Disease.

SummaryBackgroundThe aim was to evaluate the association of plasma 25-hydroxyvitamin D (25-OHD) and vitamin D binding protein (VDBP or Gc-globin) gene polymorphism with oxidant-antioxidant profiles in patients with chronic obstructive pulmonary disease (COPD), and their role as biomarker risk factors in susceptibility and severity of COPD.MethodsEighty patients diagnosed with COPD (mild, moderate and severe according to lung function tests; FEV 1%) and 80 healthy controls were included in the study. Serum nitric oxide (NO) and lipid peroxide (LP), plasma reduced glutathione (RGSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activity, 25-OHD and VDBP polymorphism were analyzed in all subjects.ResultsCOPD patients had significantly decreased serum NO, plasma SOD, RGSH, GSH-Px, CAT and 25-OHD versus controls, but had significantly increased serum LP. In COPD patients, 25-OHD levels were significantly lower (41.49± 13.65 ng/mL) versus controls, but more lower in severe COPD patients (30.54±9.09 ng/mL; sensitivity 79.2%; spe - cificity 73.2%, p<0.001) versus mild and moderate COPD. VDBP genotypes frequencies were Gc1S-1S=23.8%, Gc1F-1S=28.8%, Gc1F-1F=15%, Gc1S-2=20%, Gc1F-2=11.3% and Gc2-2=1.3%. Also, VDBP variants frequencies were Gc1S=48.1%, Gc1F=35% and Gc2=16.6%. How ever, Gc1F-1S genotypes and Gc1F variants were significantly higher than in controls (10%, 12.5%; p=0.009, p=0.001, respectively). Moreover, in severe COPD patients, Gc1F-1S genotype was significantly higher than in mild COPD (41.7% vs 31.3%, p=0.04).ConclusionCOPD patients had significantly lower plasma 25-OHD and were associated with significantly higher VDBP Gc1F-1S genotypes and Gc1F variants frequencies than controls. Low vitamin D levels and VDBP polymorphism may be important as diagnostic risk factors in the susceptibility to and severity of COPD.

Efeito do óleo de semente de uva prensado a frio nos marcadores bioquímicos e perfil inflamatório de ratos

Objetivo: O objetivo deste trabalho foi avaliar o efeito do consumo crônico do óleo de semente de uva, obtido do mercado brasileiro, nos marcadores bioquímicos e inflamatórios de ratos saudáveis. Métodos: Ratos Wistar, recém-desmamados e saudáveis, receberam por 65 dias óleo de semente de uva e soja em duas concentrações (3 e 6 mL/kg de peso corporal). Os parâmetros avaliados foram a ingestão alimentar, peso corporal e dos tecidos hepático, cerebral e adiposo retroperitonial; neste último, foi ainda realizado o perfil de ácidos graxos. A análise dos parâmetros bioquímicos, peroxidação lipídica e perfil inflamatório através da quantificação das citocinas TNF-α, IL-10 e IL-6 foi realizada no soro. Resultados: O óleo de semente de uva, independentemente da dose administrada, promoveu maior acúmulo de gordura no tecido hepático e aumento nos níveis de peroxidação lipídica do soro. Verificou-se que, quando consumido na maior dose, houve maior incorporação do ácido graxo linoleico no tecido adiposo retroperitonial. Modificações nos parâmetros bioquímicos e inflamatórios séricos não foram observadas. Conclusão: O consumo de óleo de semente de uva não provocou alterações metabólicas significantes em nenhuma das doses administradas ainda que se tenha observado uma elevação nos níveis de peroxidação lipídica sérica.

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis.

The aim of this study was to examine the oxidative status in Egyptian patients suffering chronic fascioliasis. The relationship between serum malondialdehyde (MDA) levels, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities was investigated in relation to the level of liver enzymes; ALT and AST compared to healthy controls. Twenty patients versus ten controls were included in the study. Among cases the MDA, CAT, AST and ALT were higher than controls, while SOD and GPX higher values were present among controls. There was a highly significant difference between cases and controls as regard MDA, CAT, SOD, GPX, and AST, and a significant difference regarding ALT. The findings of increased serum lipid peroxidation and decreased antioxidant enzymes in erythrocytes of chronic fascioliasis patients indicated the presence of persistent inflammation and oxidative stress which confirms the underlying pathogenesis and reflected the stage of infection providing a baseline data for comparison between normal and infected patients guided by the level of liver enzymes in relation to oxidative status.

Protective Effect of Brazilian Propolis against Liver Damage with Cholestasis in Rats Treated withα-Naphthylisothiocyanate

We examined the protective effect of Brazilian propolis against liver damage with cholestasis in rats treated with α-naphthylisothiocyanate (ANIT) in comparison with that of vitamin E (VE). Rats orally received Brazilian propolis ethanol extract (BPEE) (25, 50, or 100 mg/kg), VE (250 mg/kg) or vehicle at 12 h after intraperitoneal injection of ANIT (75 mg/kg) and were killed 24 h after the injection. Vehicle-treated rats showed liver cell damage and cholestasis, judging from the levels of serum marker enzymes and components. The vehicle group had increased serum total cholesterol, triglyceride, phospholipid, and lipid peroxide levels, increased hepatic lipid peroxide, reduced glutathione, and ascorbic acid levels and myeloperoxidase activity, and decreased hepatic superoxide dismutase activity. BPEE (50 mg/kg) administered to ANIT-treated rats prevented liver cell damage and cholestasis and attenuated these serum and hepatic biochemical changes except hepatic ascorbic acid, although administered BPEE (25 or 100 mg/kg) was less effective. VE administered to ANIT-treated rats prevented liver cell damage, but not cholestasis, and attenuated increased serum lipid peroxide level, increased hepatic lipid peroxide level and myeloperoxidase activity, and decreased hepatic superoxide dismutase activity. These results indicate that BPEE protects against ANIT-induced liver damage with cholestasis in rats more effectively than VE.

Modulation of the effects of methylmercury on rat neurodevelopment by co-exposure with Labrador Tea (Rhododendron tomentosum ssp. subarcticum)

Seafood is an important source of nutrients for many populations worldwide. Unfortunately the contamination of seafood with methylmercury (MeHg) has raised health concerns, particularly for developing infants. The modification of MeHg toxicity by nutrients, including antioxidants, has been reported in both epidemiological and animal exposure studies. We used a rat perinatal exposure model to investigate the modulation of developmental MeHg toxicity by an extract of Rhododendron tomentosum ssp. subarcticum, a plant rich in antioxidants traditionally consumed by Inuit. Sprague–Dawley rat dams were exposed daily to 2mg MeHg/kg bw and 100mg R. tomemtosum extract/kg bw administered either separately or jointly, from the first day of gestation until weaning. MeHg exposure was associated with impaired pup growth and survival, decreased grip strength, hyperactivity and altered exploratory behaviour, delayed acoustic startle response, elevated brain N-methyl-d-aspartate receptor (NMDA-R) levels, and increased serum lipid peroxidation. R. tomemtosum extract co-exposure modulated MeHg’s effects on oxidative stress and brain NMDA-R levels and may have affected MeHg pharmacokinetic. However, modulation of these molecular endpoints did not lead to significant alterations of MeHg’s effects on rat neurobehaviour.

Blockade of endogenous tissue kallikrein aggravates renal injury by enhancing oxidative stress and inhibiting matrix degradation.

Levels of tissue kallikrein (TK) are significantly lower in the urine of patients with kidney failure, and TK expression is specifically diminished in rat kidney after recovery from ischemia-reperfusion injury. In this study, we investigated the functional consequence of blocking endogenous TK activity in a rat model of chronic kidney disease. Inhibition of endogenous TK levels for 10 days by neutralizing TK antibody injection in DOCA-salt rats caused a significant increase in blood urea nitrogen and urinary protein levels, and a decrease in creatinine clearance. Kidney sections from anti-TK antibody-treated rats displayed a marked rise in tubular dilation and protein cast accumulation as well as glomerular sclerosis and size. TK blockade also increased inflammatory cell infiltration, myofibroblast and collagen accumulation, and collagen fraction volume. Elevated renal inflammation and fibrosis by anti-TK antibody were associated with increased expression of tumor necrosis factor-alpha, intercellular adhesion molecule-1, tissue inhibitor of metalloproteinase-2 (TIMP-2), and plasminogen activator inhibitor-1 (PAI-1). Moreover, the detrimental effect of TK blockade resulted in reduced nitric oxide (NO) levels as well as increased serum lipid peroxidation, renal NADH oxidase activity, and superoxide formation. In cultured proximal tubular cells, TK inhibited angiotensin II-induced superoxide production and NADH oxidase activity via NO formation. In addition, TK markedly increased matrix metalloproteinase-2 activity with a parallel reduction of TIMP-2 and PAI-1 synthesis. These findings indicate that endogenous TK has the propensity to preserve kidney structure and function in rats with chronic renal disease by inhibiting oxidative stress and activating matrix degradation pathways.

Vitamin C intake inhibits serum lipid peroxidation and osteoclast differentiation on alveolar bone in rats fed on a high-cholesterol diet

Objective A high-cholesterol diet stimulates osteoclast differentiation, which may be induced by increased serum lipid peroxidation. The inhibition of serum lipid peroxidation by vitamin C may offer beneficial effects on osteoclast differentiation including increased expression of receptor activator of nuclear factor (NF)-κB ligand (RANKL) and NF-κB. This study investigated the effects of vitamin C intake on RANKL and NF-κB expression in periodontal tissue of rats fed a high-cholesterol diet. Design Twenty-four rats (8 weeks old) were divided into four groups: a control group (fed a regular diet) and three experimental groups (fed a high-cholesterol diet supplemented with 0, 1 and 2 g/l vitamin C/day) in this 12-week study. Vitamin C was provided by its addition to drinking water. As an index of serum lipid peroxidation, hexanoyl-lysine (HEL) level was determined by a competitive enzyme-linked immunosorbent assay method. Immunohistological analysis was performed to evaluate RANKL and NF-κB expression on the alveolar bone surface. The number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts was also counted. Results Feeding a high-cholesterol diet increased not only the serum HEL level but also the number of TRAP-positive osteoclasts on the alveolar bone surface, with an increase in RANKL and NF-κB expression on alveolar bone surface. Intake of vitamin C reduced the serum HEL level and osteoclast differentiation, with decreasing RANKL and NF-κB expression. Conclusions Vitamin C intake could suppress osteoclast differentiation, including RANKL and NF-κB expression on the alveolar bone surface, by decreasing serum lipid peroxidation in rats fed a high-cholesterol diet.

Magnesium attenuates isoproterenol-induced acute cardiac dysfunction and β-adrenergic desensitization

Sympathetic nervous activation is a crucial compensatory mechanism in heart failure. However, excess catecholamine may induce cardiac dysfunction and beta-adrenergic desensitization. Although magnesium is known to be a cardioprotective agent, its beneficial effects on acute cardiac dysfunction remain to be elucidated. We examined the effects of magnesium on left ventricular (LV) dysfunction induced by a large dose of isoproterenol in dogs. Sixteen anesthetized dogs underwent a continuous infusion of isoproterenol (1 micro g.kg(-1).min(-1)) with or without a magnesium infusion (1 mg.kg(-1).min(-1)). The dose response to small doses of isoproterenol (0.025-0.2 micro g.kg(-1).min(-1)) was tested hourly. A large dose of isoproterenol decreased LV systolic function, increased the time constant of LV isovolumic relaxation, and suppressed the dose response to small doses of isoproterenol in a time-dependent manner. Magnesium significantly attenuated isoproterenol-induced LV systolic and diastolic dysfunction and preserved the dose response to isoproterenol. Serum-ionized calcium significantly decreased with a large dose of isoproterenol but was fully maintained at baseline level with magnesium. A large dose of isoproterenol increased serum lipid peroxide levels and serological markers of myocardial damage, which were significantly suppressed by magnesium. In conclusion, magnesium significantly attenuated excess isoproterenol-induced acute cardiac dysfunction and beta-adrenergic desensitization.

Combined effect of probucol and insulin on cataracts of diabetic rats fed a high cholesterol diet

We investigated the effects of long-term treatment with probucol, a hypolipidemic agent with antioxidative action, insulin, or their combination on cataracts of streptozotocin-induced diabetic rats fed a high cholesterol diet. Each rat was checked for cataracts at 0, 1, 2, 4, 8, 12 and 15 weeks after streptozotocin injection. Cataracts were observed from 8 weeks in untreated hypercholesterolemic and diabetic rats and the incidence of catarats increased to 100% by 15 weeks. The incidence of cataracts in rats treated with probucol, insulin and their combination was first seen at 12, 12 and 15 weeks, respectively, and was 86%, 63% and 33%, respectively, at 15 weeks. The preventive effects of both agents alone and their combination on the cataracts were confirmed by histopathological evaluation of eyeballs. The combined treatment with both agents markedly improved hyperglycemia, hyperlipidemia and increased serum lipid peroxide levels. These results indicate that the combined treatment with probucol and insulin is useful in preventing the development and progression of diabetic cataracts.

Inhibitory effects of water extracts from fruiting bodies of cultured Cordyceps sinensis on raised serum lipid peroxide levels and aortic cholesterol deposition in atherosclerotic mice.

We investigated the effects of the water extracts of the fruiting bodies of cultured Cordyceps sinensis (WECS) on lipid metabolism in mice fed an atherogenic diet. WECS was orally administered at doses of 50, 100 and 200 mg/kg/day for 12 weeks. WECS showed no toxic effects on the growth rate, liver or kidney weights of the mice. Mice fed the atherogenic diet showed marked increases in serum lipid and lipid peroxide levels and also aortic cholesterol levels, particularly cholesteryl ester level, a major lipid constituent in atherosclerotic lesions. WECS significantly suppressed the increased serum lipid peroxide level but not other lipid levels in a dose-dependent manner. WECS also suppressed the increased aortic cholesteryl ester level in a dose-dependent manner. These results suggest that WECS prevents cholesterol deposition in the aorta by inhibition of LDL oxidation mediated by free radicals rather than by reduction in serum lipid level. WECS may exert beneficial effects on the formation of the atherosclerotic lesion induced by oxidative stress with few side effects.

Increase with age of serum lipid peroxides: Implications for the prevention of atherosclerosis

There is considerable support for the concept that oxygen free radicals and related lipid peroxides play a key role in the pathogenesis of normal senescence and of age-related chronic degenerative diseases, including atherosclerosis. This has led to a great deal of interest regarding peroxidized LDL, which seems to be more atherogenic than LDL. In contrast, the relationship of total serum or plasma lipid peroxides (which also have a marked atherogenic action) with both aging and atherogenesis are not well understood. In view of the above, we have determined the level of serum lipid peroxide (expressed as thiobarbituric acid reactive substances) in a sample of 100 healthy men and women ranging in age from 20 to 70 years. Our data show that there is an age related increase in the concentration of lipid peroxide, with men showing higher or about equal values than women until about 60 years, after which age women show the higher values. Our data also suggest that in certain men and women, aging is linked to a decline in the competence of the oxyradical-detoxifying mechanisms, which results in increased serum lipid peroxidation. Further research is needed to find out if lowering the serum peroxide levels of aging subjects by diet supplementation with antioxidants will decrease that risk. An adequate intake of antioxidants seems especially indicated in post-menopausal women because of their apparent greater sensitivity to age related oxygen stress.

Serum Lipid Peroxide Level and Vitamin B2 Status of Pregnant Women

Serum lipid peroxide level and vitamin B2 status of 90 pregnant (27 in the 1st trimester, 23 in the 2nd trimester, and 40 in the 3rd trimester) and 33 healthy non-pregnant women were examined.Serum lipid peroxide level of the pregnant women increased as pregnancy progressed, and the level at the 3rd trimester was significantly higher than that of the non-pregnant women. Thirty pregnant women had an increase in serum lipid peroxide level and 10 of them had marginal riboflavin deficiency as judged by their erythrocyte glutathione reductase (EGR) activity coefficients. The number of pregnant women having both increased serum lipid peroxide level and marginal riboflavin deficiency increased with the advancement of pregnancy (0 in the 1st trimester, 1 in the 2nd trimester, and 9 in the 3rd trimester). A weak positive correlation between serum lipid peroxide level and EGR activity coefficient of the pregnant women was found in the 3rd trimester. These results indicate that the increase in serum lipid peroxide level during pregnancy, particularly at the late stage, may be at least partly attributable to marginal riboflavin deficiency.