Isoflavone-Rich Soy Isolate Reduces Lipid Peroxidation in Mouse Liver

2008 ◽  
Vol 78 (45) ◽  
pp. 217-222 ◽  
Author(s):  
Wissam H. Ibrahim ◽  
Hosam M. Habib ◽  
Ching K. Chow ◽  
Geza G. Bruckner
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Glutathione Peroxidase ◽  
Membrane Lipids ◽  
Basal Diet ◽  
Conjugated Dienes ◽  
Control Group ◽  
Peroxidative Damage ◽  
Soy Isolate

The purpose of this study was to determine if an isoflavone-rich soy isolate affords protection against peroxidative damage in vivo. Weanling C57BL6 male mice were fed a basal diet (AIN-93G) supplemented with either nothing or 1.08 gram isoflavone-rich soy isolate/kg diet for 60 days. The soy isolate contained 400 mg/g isoflavone aglycones (226 mg/g genistein and 174 mg/g daidzein). Immediately following sacrifice liver was processed for measuring the levels of lipid peroxidation products, malondialdehyde (MDA) and conjugated dienes, and the levels of α-tocopherol, glutathione (GSH), and ascorbic acid, as well as the activities of catalase, selenium-dependent glutathione peroxidase (Se-GPx), selenium-nondependent glutathione peroxidase (non-Se-GPx), and superoxide dismutase (SOD). Compared with the control group, mice fed the diet supplemented with soy isolate had significantly (p < 0.05) lower hepatic levels of MDA and conjugated dienes. The activities of catalase and SOD were significantly increased (p < 0.05) in the liver of soy isolate-supplemented mice. The levels of vitamin E, GSH, and ascorbic acid and the activities of Se-GPx and non-Se-GPx were not significantly altered by the soy isolate. The results obtained provide experimental evidence that isoflavone supplementation confers protection against peroxidative damage to membrane lipids in vivo, possibly through enhancing the activities of the antioxidant enzymes catalase and SOD.

scholarly journals Iron loading and large doses of intravenous ascorbic acid promote lipid peroxidation in whole serum in guinea pigs

2001 ◽  
Vol 85 (6) ◽  
pp. 681-687 ◽  
Author(s):  
Maria Kapsokefalou ◽  
Dennis D Miller
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Guinea Pigs ◽  
Intraperitoneal Injection ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Iron Dextran ◽  
Cardiac Puncture

Large doses of ascorbic acid may mobilise Fe from Fe-binding proteins in vivo which in turn could catalyse lipid peroxidation, a process associated with degenerative diseases. This hypothesis was tested in vitro in the serum of Fe-loaded animals. Eighteen male guinea pigs weighing about 500 g on arrival were allocated to two groups of nine. Fe loading was induced in one group by two intraperitoneal injections of 200 mg iron dextran given on days 1 and 5. Blood (6 ml) was drawn from all animals on day 12 by cardiac puncture. Serum and LDL were separated. Serum was tested for loosely-bound Fe (bleomycin assay) and lipid peroxidation (thiobarbituric acid reactive substances (TBARS) assay) and LDL for susceptibility to in vitro oxidation (TBARS and conjugated diene assays). On day 12, another intraperitoneal injection of 200 mg iron dextran was given to the animals in the Fe-loaded group. On day 19, all animals were given 75 mg ascorbic acid by intraperitoneal injection. Blood (6 ml) was drawn 4 h later by cardiac puncture. Serum and LDL assays were repeated. Ascorbic acid increased loosely-bound Fe and in vitro oxidation in the serum from animals of the Fe-loaded group but not in the serum from animals of the control group. Susceptibility of LDL to in vitro oxidation increased after the ascorbic acid injection in the control group but there was no further increase in the Fe-loaded group. These data suggest that large doses of ascorbic acid promote Fe mobilisation and in vitro oxidation in the serum of Fe-loaded animals.

State of the enzyme link of antioxidant protection in boys with hypoandrogenism

2020 ◽  
Vol 40 (4) ◽  
pp. 32-36
Author(s):  
L. K. Parkhomenko ◽  
◽  
L. A. Strashok ◽  
S. I. Turchina ◽  
G. V. Kosovtsova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Free Radical ◽  
Glutathione Peroxidase ◽  
Free Radical Oxidation ◽  
Conjugated Dienes ◽  
Delayed Puberty ◽  
Control Group ◽  
Antioxidant Protection ◽  
Radical Oxidation

Recently, interest in the problem of free radical oxidation in biological membranes, which is directly related to both the normal functioning of cells and the occurrence, course and outcome of many pathological conditions, has increased again in clinical medicine. The aim was to determine the role and impact of antioxidant defense in boys with hypoandrogenism. The study involved 75 adolescents with hypoandrogenism aged 13–18 years, who underwent a complex of clinical and laboratory examinations. All patients were conducted complex of anthropometric research and determination of the degree of delayed puberty, laboratory and instrumental examination. Free radical oxidation was determined by the levels of malondialdehyde, conjugated dienes, carbonated proteins, superoxide dismutase and catalase in the serum, and restored glutathione and glutathione peroxidase in whole blood. Based on their determination, the coefficient of oxidative stress was calculated. Statistical processing of results was performed using parametric and nonparametric methods. The study of indicators of the free radical oxidation process found that adolescents with hypoandrogenism have multidirectional changes in the oxidation of proteins and lipids, namely: the level of conjugated dienes increases, the concentration of malondialdehyde remains at the level of the control group, and the level of carbonated proteins tends to decrease. As for the activity of antioxidant protection enzymes, a significant decrease in the level of glutathione peroxidase was detected, while the level of superoxide dismutase and catalase remained at the level of normative indicators. Oxidative stress accompanies and is one of the pathogenetic links in the formation or maintenance of the state of hypoandrogenism in boys. This requires the use of antioxidants, the complex of which must be selected individually.

Exercise training improves myocardial tolerance to in vivo ischemia-reperfusion in the rat

1998 ◽  
Vol 275 (5) ◽  
pp. R1468-R1477 ◽  
Author(s):  
Scott K. Powers ◽  
Haydar A. Demirel ◽  
Heather K. Vincent ◽  
Jeff S. Coombes ◽  
Hisashi Naito ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Experimental Studies ◽  
Control Group ◽  
Sprague Dawley ◽  
Endurance Exercise Training ◽  
Nonprotein Thiols

Experimental studies examining the effects of regular exercise on cardiac responses to ischemia and reperfusion (I/R) are limited. Therefore, these experiments examined the effects of endurance exercise training on myocardial biochemical and physiological responses during in vivo I/R. Female Sprague-Dawley rats (4 mo old) were randomly assigned to either a sedentary control group or to an exercise training group. After a 10-wk endurance exercise training program, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was achieved by a ligature around the left coronary artery; occlusion was maintained for 20 min, followed by a 10-min period of reperfusion. Compared with untrained, exercise-trained animals maintained higher ( P < 0.05) peak systolic blood pressure throughout I/R. Training resulted in a significant ( P < 0.05) increase in ventricular nonprotein thiols, heat shock protein (HSP) 72, and the activities of superoxide dismutase (SOD), phosphofructokinase (PFK), and lactate dehydrogenase. Furthermore, compared with untrained controls, left ventricles from trained animals exhibited lower levels ( P < 0.05) of lipid peroxidation after I/R. These data demonstrate that endurance exercise training improves myocardial contractile performance and reduces lipid peroxidation during I/R in the rat in vivo. It appears likely that the improvement in the myocardial responses to I/R was related to training-induced increases in nonprotein thiols, HSP72, and the activities of SOD and PFK in the myocardium.

Phytochemical analysis and nephroprotective effect of cactus (Opuntia ficus-indica) cladodes on sodium dichromate-induced kidney injury in rats

2019 ◽  
Vol 44 (3) ◽  
pp. 239-247
Author(s):  
Mbarka Hfaiedh ◽  
Dalel Brahmi ◽  
Mohamed Nizar Zourgui ◽  
Lazhar Zourgui
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Wistar Rat ◽  
Phytochemical Analysis ◽  
Sodium Dichromate ◽  
Opuntia Ficus Indica

Environmental and occupational exposure to chromium compounds, especially hexavalent chromium, is widely recognized as potentially nephrotoxic in humans and animals. The present study aimed to assess the efficacy of cactus (Opuntia ficus-indica) against sodium dichromate-induced nephrotoxicity, oxidative stress, and genotoxicity. Cactus cladodes extract (CCE) was phytochemically studied and tested in vitro for its potential antioxidant activities. Additionally, the preventive effect of CCE against sodium dichromate-induced renal dysfunction in a Wistar rat model (24 rats) was evaluated. For this purpose, CCE at a dose of 100 mg/kg was orally administered, followed by 10 mg/kg sodium dichromate (intraperitoneal injection). After 40 days of treatment, the rats were sacrificed, and the kidneys were excised for histological, lipid peroxidation, and antioxidant enzyme analyses. The phenol, flavonoid, tannin, ascorbic acid, and carotenoid contents of CCE were considered to be important. Our analyses showed that 1 mL of CCE was equivalent to 982.5 ± 1.79 μg of gallic acid, 294.37 ± 0.84 μg of rutin, 234.78 ± 0.24 μg of catechin, 204.34 ± 1.53 μg of ascorbic acid, and 3.14 ± 0.51 μg of β-carotene. In vivo, pretreatment with CCE was found to provide significant protection against sodium dichromate-induced nephrotoxicity by inhibiting lipid peroxidation, preserving normal antioxidant activities, and protecting renal tissues from lesions and DNA damage. The nephroprotective potential of CCE against sodium dichromate toxicity might be due to its antioxidant properties.

Lipid peroxidation and antielastase activity in the lung under oxidant stress: role of antioxidant defenses

1991 ◽  
Vol 70 (4) ◽  
pp. 1456-1462 ◽  
Author(s):  
V. Mohsenin
Keyword(s):  
Lipid Peroxidation ◽  
Oxidant Stress ◽  
Lavage Fluid ◽  
Conjugated Dienes ◽  
Antioxidant Defenses ◽  
Vitamin Supplementation ◽  
Control Group ◽  
Early Event ◽  
Lipid Peroxidation Products

The role of lipid peroxidation in the inactivation of alpha 1-protease inhibitor (alpha 1-PI) in the alveolar lining fluid of human subjects has been examined under oxidant stress. Exposure to nitrogen dioxide (NO2) at 4 ppm for 3 h resulted in a significant increase in the amount of lipid peroxidation products in the alveolar lining fluid, with conjugated dienes the predominant species. Four-week supplementation with vitamins C and E before NO2 exposure markedly decreased the levels of conjugated dienes (control 804 +/- 103 pmol/micrograms total phospholipids vs. vitamin-supplemented 369 +/- 58, P = 0.003). Malondialdehydes, although detectable in the lavage fluid, contributed little to the total amount of lipid peroxidation products, and the levels were comparable in both groups. NO2 exposure in the absence of vitamin supplementation caused a significant decrease in the elastase inhibitory capacity (EIC) of the alveolar lining fluid in the control group but not in the vitamin-supplemented group [control 3.67 +/- 0.32 micrograms alpha 1-PI/micrograms porcine pancreatic elastase (PPE) vs. vitamin-supplemented 2.75 +/- 0.17, P less than 0.03]. The vitamin-supplemented group had a lower level of conjugated dienes and a higher EIC. Conversely, the control group had higher levels of conjugated dienes and a lower EIC in their lavage fluid. These studies demonstrate that lipid peroxidation occurs as an early event during oxidant exposure in the lungs of normal subjects. The appearance of lipid peroxidation products in the lavage fluid is associated with a decrease in the EIC of the alveolar lining fluid. Vitamins C and E diminish lipid peroxidation and preserve the EIC of the lower respiratory tract fluid during oxidant stress.

scholarly journals Histochemical examination on principal collagen fibers in periodontal ligaments of ascorbic acid-deficient ODS-od/od rats

Microscopy ◽  
2019 ◽  
Vol 68 (5) ◽  
pp. 349-358 ◽  
Author(s):  
Tomoka Hasegawa ◽  
Yukina Miyamoto-Takasaki ◽  
Miki Abe ◽  
Zixuan Qiu ◽  
Tomomaya Yamamoto ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Acid Solution ◽  
Collagen Fibers ◽  
Collagen Fibrils ◽  
Male Rats ◽  
Control Group ◽  
Ascorbic Acid Solution ◽  
Cathepsin H ◽  
Periodontal Ligaments

Abstract In this study, we aimed to clarify the role of ascorbic acid in collagen synthesis in periodontal ligaments using osteogenic disorder Shionogi (ODS)/ShiJcl-od/od rats lacking L-gulonolactone oxidase. These rats cannot synthesize ascorbic acid in vivo. Eight-week-old ODS/ShiJcl-od/od male rats were administered ascorbic acid solution at a concentration of 200 mg/dL (control group, n = 6) or ascorbic acid solution at concentration of 0.3 mg/dL (insufficient group, n = 12). Six rats of the insufficient group were then given with ascorbic acid solution at concentration of 200 mg/dL for additional 3 weeks (rescued group, n = 6), and then, their mandibles were histochemically examined. Consequently, the insufficient group specimens were seen to possess fewer collagen fibers, and silver impregnation revealed numerous fine, reticular fiber-like fibrils branching off from collagen in the periodontal ligaments. In control group, faint immunoreactivities for matrix metalloproteinase (MMP)2 and cathepsin H were seen in the periphery of blood vessels and throughout the ligament, respectively. In contrast, in the insufficient group, intense MMP2-immunoreactivity was observed to be associated with collagen fibrils in the periodontal ligaments, and cathepsin H-immunopositivity was seen in ligamentous cells. The rescued group showed abundant collagen fibers filling the periodontal ligament space. Under transmission electron microscopy, ligamentous fibroblasts incorporated collagen fibrils into tubular endosomes/lysosomes while simultaneously synthesizing collagen fibril bundles. Thus, ascorbic acid insufficiency affected the immunolocalization of cathepsin H and MMP2; however, ligamentous fibroblasts appear to possess the potential to synthesize collagen fibers when supplied with ascorbic acid.

Oxidative stress and platelet activation in subjects with moderate hyperhomocysteinaemia due to MTHFR 677 C→T polymorphism

2012 ◽  
Vol 108 (09) ◽  
pp. 533-542 ◽  
Author(s):  
Alfredo Dragani ◽  
Angela Falco ◽  
Francesca Santilli ◽  
Stefania Basili ◽  
Giancarlo Rolandi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Folic Acid ◽  
Platelet Activation ◽  
Methylenetetrahydrofolate Reductase ◽  
Folic Acid Supplementation ◽  
Control Group ◽  
Loading Test ◽  
Study Objective ◽  
Acid Supplementation

SummaryThe methylenetetrahydrofolate reductase (MTHFR) 677 C→T polymorphism may be associated with elevated total homocysteine (tHcy) levels, an independent risk factor for cardiovascular disease. It was the study objective to evaluate in vivo lipid peroxidation and platelet activation in carriers of the MTHFR 677 C→T polymorphism and in non-carriers, in relation to tHcy and folate levels. A cross-sectional comparison of urinary 8-iso-prostaglandin (PG)F2α and 11-dehydro-thromboxane (TX)B2 (markers of in vivo lipid peroxidation and platelet activation, respectively) was performed in 100 carriers and 100 non-carriers of the polymorphism. A methionine-loading test and folic acid supplementation were performed to investigate the causal relationship of the observed associations. Urinary 8-iso-PGF2α and 11-dehydro-TXB2 were higher in carriers with hyperhomocysteinaemia than in those without hyperhomocysteinaemia (p<0.0001). Hyperhomocysteinaemic carriers had lower folate levels (p=0.0006), higher urinary 8-iso-PGF2α (p<0.0001) and 11-dehydro-TXB2 (p<0.0001) than hyperhomocysteinaemic non-carriers. On multiple regression analysis, high tHcy (p<0.0001), low folate (p<0.04) and MTHFR 677 C→T polymorphism (p<0.001) independently predicted high rates of 8-iso-PGF2α excretion. Methionine loading increased plasma tHcy (p=0.002), and both urinary prostanoid metabolites (p=0.002). Folic acid supplementation was associated with decreased urinary 8-iso-PGF2α and 11-dehydro-TXB2 excretion (p<0.0003) in the hyperhomocysteinaemic group, but not in the control group, with substantial inter-individual variability related to baseline tHcy level and the extent of its reduction. In conclusion, hyperhomocysteinaemia due to the MTHFR 677 C→T polymorphism is associated with enhanced in vivo lipid peroxidation and platelet activation that are reversible, at least in part, following folic acid supplementation. An integrated biomarker approach may help identifying appropriate candidates for effective folate supplementation.

scholarly journals In VivoAntioxidant Activity of Deacetylasperulosidic Acid in Noni

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
De-Lu Ma ◽  
Mai Chen ◽  
Chen X. Su ◽  
Brett J. West
Keyword(s):  
Antioxidant Activity ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Catalase Activity ◽  
Antioxidant Properties ◽  
Superoxide Dismutase Activity ◽  
Morinda Citrifolia ◽  
Control Group ◽  
Dose Dependent

Deacetylasperulosidic acid (DAA) is a major phytochemical constituent ofMorinda citrifolia(noni) fruit. Noni juice has demonstrated antioxidant activityin vivoand in human trials. To evaluate the role of DAA in this antioxidant activity, Wistar rats were fed 0 (control group), 15, 30, or 60 mg/kg body weight per day for 7 days. Afterwards, serum malondialdehyde concentration and superoxide dismutase and glutathione peroxidase activities were measured and compared among groups. A dose-dependent reduction in malondialdehyde was evident as well as a dose-dependent increase in superoxide dismutase activity. DAA ingestion did not influence serum glutathione peroxidase activity. These results suggest that DAA contributes to the antioxidant activity of noni juice by increasing superoxide dismutase activity. The fact that malondialdehyde concentrations declined with increased DAA dose, despite the lack of glutathione peroxidase-inducing activity, suggests that DAA may also increase catalase activity. It has been previously reported that noni juice increases catalase activityin vivobut additional research is required to confirm the effect of DAA on catalase. Even so, the current findings do explain a possible mechanism of action for the antioxidant properties of noni juice that have been observed in human clinical trials.

Effect of Dietary Selenite on Hepatic Organic Solvent-Soluble Lipofuscin Pigments

1986 ◽  
Vol 5 (1) ◽  
pp. 79-85 ◽  
Author(s):  
A.S. Csallany ◽  
B.Z. Menken
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Organic Solvent ◽  
Normal Level ◽  
Sodium Selenite ◽  
Basal Diet ◽  
Glutathione Peroxidase Activity ◽  
End Products ◽  
Oxidative Effect

Supplementation of selenium as sodium selenite results in an increase in hepatic organic solvent-soluble lipofuscin pigments, the metabolic end products of lipid peroxidation. Weanling mice fed a basal diet containing 0.05 ppm selenium had a significant increase in hepatic organic solvent-soluble lipofuscin pigments and glutathione peroxidase activity following supplementation of an additional 0.1 ppm selenium as sodium selenite from 5 to 9 months of age. Normal levels of vitamin E (30 mg/kg) were insufficient to protect against the oxidative effect of this increased dose of selenite. However, 10 times the normal level of vitamin E markedly suppressed this oxidative effect.

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