Alpha-Tocopherol and the Lipid Peroxidation Regulation in Murine Tissues Under Acute Irradiation

2013 ◽  
pp. 505-520
Keyword(s):  
Lipid Peroxidation ◽  
Alpha Tocopherol ◽  
Acute Irradiation

Oxygen free radical-mediated selective endothelial dysfunction in isolated coronary artery

1992 ◽  
Vol 262 (3) ◽  
pp. H806-H812 ◽  
Author(s):  
K. Todoki ◽  
E. Okabe ◽  
T. Kiyose ◽  
T. Sekishita ◽  
H. Ito
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Free Radical ◽  
Coronary Artery ◽  
Iron Chelator ◽  
Oxygen Free Radical ◽  
Alpha Tocopherol ◽  
Endothelium Dependent Relaxation ◽  
Iron Chelator Deferoxamine

To understand the direct involvement of free radicals causing reduction in endothelium-dependent relaxation of isolated canine coronary ring preparations, this study was undertaken to examine the effect of free radicals generated from dihydroxy fumarate (DHF) plus Fe(3+)-ADP or from H2O2 plus FeSO4. The vasodilators (acetylcholine, bradykinin, A23187, and nitroglycerin) were given after DHF/Fe(3+)-ADP or H2O2/FeSO4 was removed from the organ chamber. The earlier DHF/Fe(3+)-ADP exposure produced an attenuation of the relaxation of the rings induced by acetylcholine, bradykinin, or A23187 but not of the relaxation induced by nitroglycerin. The observed effect of previous DHF/Fe(3+)-ADP exposure was significantly protected in the vessels isolated from the dogs treated with alpha-tocopherol. In the experiments for assessing the effect of various scavengers, 1O2 scavenger histidine or iron chelator deferoxamine effectively protected the attenuation induced by DHF/Fe(3+)-ADP exposure of the relaxation elicited by acetylcholine; superoxide dismutase (SOD), catalase, or dimethyl sulfoxide (DMSO) had no effect on this system. Furthermore, the relaxation elicited by acetylcholine, but not nitroglycerin, was significantly attenuated by the earlier exposure to .OH generated by Fenton's reagent (H2O2+FeSO4); the attenuation was significantly protected by DMSO. These results are consistent with the view that .OH, 1O2, and/or iron-dependent reactive species selectively damage endothelium-dependent relaxation as opposed to endothelium-independent relaxation in endothelium-intact coronary ring preparations. It is also postulated that lipid peroxidation may be responsible for this effect.

Skeletal muscle lipid peroxidation in exercised and food-restricted rats during aging

1989 ◽  
Vol 67 (1) ◽  
pp. 69-75 ◽  
Author(s):  
J. W. Starnes ◽  
G. Cantu ◽  
R. P. Farrar ◽  
J. P. Kehrer
Keyword(s):  
Lipid Peroxidation ◽  
Gastrocnemius Muscle ◽  
Thiobarbituric Acid ◽  
Exercise Group ◽  
Alpha Tocopherol ◽  
Treadmill Running ◽  
Control Group ◽  
Muscle Lipid ◽  
Fischer 344 ◽  
Skeletal Muscle Lipid

The effects of chronic endurance exercise and food restriction on nonenzymatic lipid peroxidation (LP) of gastrocnemius muscle during aging were studied in male, Fischer 344 rats. One set of rats aged 6 and 18 mo were assigned to an exercise group (treadmill running) or an age-matched sedentary control group. After 6 mo (at the ages of 12 and 24 mo), LP and levels of alpha-tocopherol and its oxidized form, alpha-tocopheryl quinone, were measured. The extent of LP was determined in homogenates by measuring the content of thiobarbituric acid-reactive substances. After homogenization, the muscles were immediately evaluated for basal LP and also incubated in the presence of oxidant stressors for 2 h to assess antioxidant capacity (AOC) and for 24 h to estimate total peroxidizable lipid (TPL). Basal LP was not affected by age or exercise. AOC was not affected by exercise at either age. However aging significantly decreased AOC and increased alpha-tocopheryl quinone in both sedentary and exercised groups. TPL was not affected by age, but was increased by exercise training (P less than 0.05). Another set of rats was divided into the following three groups at 3 mo of age: sedentary, fed ad libitum (S); sedentary, caloric restricted by alternate day feeding (R); and exercised by forced treadmill running (E). Two years later, when the rats were 27 mo of age, the extent of LP was assessed.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Analysis of the relationship between hemoglobin-oxygen affinity and lipid peroxidation during fever.

1995 ◽  
Vol 42 (1) ◽  
pp. 69-74 ◽  
Author(s):  
M V Borisiuk ◽  
V V Zinchuk
Keyword(s):  
Lipid Peroxidation ◽  
Malonic Dialdehyde ◽  
Oxygen Affinity ◽  
Alpha Tocopherol ◽  
Diene Conjugates ◽  
Tocopherol Concentration ◽  
Hemoglobin Oxygen Affinity ◽  
The Relationship ◽  
Free Radical Lipid Oxidation ◽  
Oxyhemoglobin Dissociation

Endogenous hyperthermia was induced in rabbits by i.v. pyrogenal administration. Hemoglobin-oxygen affinity and parameters of free radical lipid oxidation in plasma and red blood cells were measured. The content of diene conjugates, malonic dialdehyde and Schiff bases were determined at a pyrogenal dose of 4 minimal pyrogenic doses/kg, and iron-initiated chemiluminescence, catalase activity and alpha-tocopherol concentration were determined at 6 minimal pyrogenic doses/kg. A rightward shift of the real oxyhemoglobin dissociation curve and activation of lipid peroxidation were observed. Relationships between the parameters measured were analyzed. Decreased hemoglobin-oxygen affinity is considered to be a possible mechanism of activation of free radicals during fever.

scholarly journals Wound healing potential of palm oil tocotrienols rich fraction

Food Research ◽  
2021 ◽  
Vol 5 (4) ◽  
pp. 394-403
Author(s):  
T.M. Ting ◽  
J.H. King ◽  
K.L. Ho ◽  
H.L.N. Lau
Keyword(s):  
Lipid Peroxidation ◽  
Wound Healing ◽  
Blood Glucose ◽  
Wound Closure ◽  
Diabetes Management ◽  
Gastrointestinal Symptoms ◽  
Alpha Tocopherol ◽  
Diabetic Patients ◽  
Standard Drug ◽  
Immune System Activation

Diabetic patients often experience problems with their immune system activation and result in delayed wound healing. Slow and incomplete wound healing increases the risk of complications caused by infected wounds. Metformin has been used as a standard drug for diabetes treatment and it accelerates wound healing. However, intake of metformin may cause gastrointestinal symptoms including diarrhoea, nausea and abdominal discomfort. Therefore, a safe alternative to metforminis is required. While many research programs focus on alpha-tocopherol, in this paper the potency of tocotrienols in wound and diabetes management was investigated. Tocotrienol rich fraction (TRF) was tested for its ability to stabilize blood glucose, reduce lipid peroxidation, promote platelet-derived growth factorBB and wound closure. In this study, the rodent model was used to investigate the effects of TRP in wound healing proficiency. The results showed that TRF was comparable to metformin in stabilizing blood glucose, promoting PDGF-BB in the blood during the initial wound healing stage and produced clean wound closure. Interestingly, the findings of this study showed TRF had higher potency than metformin in reducing lipid peroxidation that could delay wound healing. Hence, TRF could be a good alternative to metformin in wound and diabetes management

Alpha-tocopherol and ginkgo biloba treatment protects lipid peroxidation during ischemic period in rat groin island skin flaps

1997 ◽  
Vol 20 (3) ◽  
pp. 141-144 ◽  
Author(s):  
M. Deveci ◽  
I. Dibirdik ◽  
B. Çeliköz ◽  
N. Selmanpakoĝlu ◽  
U. Kisa
Keyword(s):  
Lipid Peroxidation ◽  
Ginkgo Biloba ◽  
Alpha Tocopherol ◽  
Skin Flaps ◽  
Ischemic Period

Vitamin E decreases hepatic levels of aldehyde-derived peroxidation products in rats with iron overload

1996 ◽  
Vol 270 (2) ◽  
pp. G376-G384 ◽  
Author(s):  
S. Parkkila ◽  
O. Niemela ◽  
R. S. Britton ◽  
K. E. Brown ◽  
S. Yla-Herttuala ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Iron Overload ◽  
Kupffer Cells ◽  
Laser Scanning ◽  
Laser Scanning Microscopy ◽  
Alpha Tocopherol ◽  
Confocal Laser ◽  
Hepatocellular Injury ◽  
Vitamin E Supplementation

Hepatic iron overload can cause lipid peroxidation with the formation of aldehydic products, hepatocellular injury, and fibrosis. Vitamin E (alpha-tocopherol) may prevent peroxidation-induced hepatic damage. We used confocal laser scanning microscopy, digital image analysis, and immunohistochemical methods to quantitate aldehyde-derived peroxidation products in the liver of rats with experimental iron overload with or without supplemental vitamin E. A strong autofluorescent reaction colocalizing with iron deposits was present in the livers of iron-loaded rats. Fluorescent granules were unevenly distributed in the cytosol of both hepatocytes and Kupffer cells in the periportal regions. Immunohistochemical studies revealed the presence of malon-dialdehyde adducts in the periportal regions of the ironloaded rats. Vitamin E supplementation markedly reduced the fluorescence intensity and the amount of aldehyde-derived peroxidation products and changed the distribution of stainable iron and iron-associated peroxidation products such that their levels were much decreased in Kupffer cells. These results indicate that aldehyde-derived covalent chemical addition products are formed in the liver in iron overload. Vitamin E supplementation markedly reduces the amount of these compounds and changes their cellular distribution. These findings should be implicated in the role of antioxidant therapy in conditions causing iron overload and lipid peroxidation.

Oxidation of alpha 1-protease inhibitor: role of lipid peroxidation products

1989 ◽  
Vol 66 (5) ◽  
pp. 2211-2215 ◽  
Author(s):  
V. Mohsenin ◽  
J. L. Gee
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Stearic Acid ◽  
Protease Inhibitor ◽  
Alpha Tocopherol ◽  
Inhibitory Capacity ◽  
Buffer Control

Previously we demonstrated that in vivo exposure of humans to NO2 resulted in significant inactivation of alpha 1-protease inhibitor (alpha 1-PI) in the bronchoalveolar lavage fluid. However, alpha 1-PI retains its elastase inhibitory activity in vitro when exposed to 10 times the concentration of NO2 used in vivo. We suggested exogenous oxidants such as O2 and NO2 exert their effect in vivo in part through lipid peroxidation. We investigated the mechanism of inactivation of alpha 1-PI in the presence or absence of lipids under oxidant atmosphere. alpha 1-PI in solutions containing phosphate buffer (control), 0.1 mM stearic acid (saturated fatty acid, 18:0), or 0.1 mM linoleic acid (polyunsaturated fatty acid, 18:2) was exposed to either N2 or NO2 (50 ppm for 4 h). Elastase inhibitory capacity of alpha 1-PI was significantly diminished in the presence of 0.1 mM linoleic acid and under NO2 atmosphere (75 +/- 8% of control, P less than 0.01), whereas there was no change in elastase inhibitory capacity of alpha 1-PI in the presence or absence (buffer only) of 0.1 mM stearic acid under a similar condition (109 +/- 11 and 94 +/- 6%, respectively). The inactivated alpha 1-PI as the result of peroxidized lipid could be reactivated by dithiothreitol and methionine sulfoxide peptide reductase, suggesting oxidation of methionine residue at the elastase inhibitory site. Furthermore the inhibitory effect of peroxidized lipid on alpha 1-PI could be prevented by glutathione and glutathione peroxidase and to some extent by alpha-tocopherol.

Dehydroepiandrosterone administration prevents the oxidative damage induced by acute hyperglycemia in rats

1997 ◽  
Vol 155 (2) ◽  
pp. 233-240 ◽  
Author(s):  
M Aragno ◽  
E Brignardello ◽  
E Tamagno ◽  
V Gatto ◽  
O Danni ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Alpha Tocopherol ◽  
Thiobarbituric Acid Reactive Substances ◽  
Acute Hyperglycemia ◽  
Tissue Resistance ◽  
In Vivo Administration ◽  
Different Doses

Free radical overproduction contributes to tissue damage induced by acute hyperglycemia. Dehydroepiandrosterone, which has recently been found to have antioxidant properties, was administered i.p. to rats at different doses (10, 50 or 100 mg/kg body weight) 3 h before treatment with dextrose (5 g/kg). Lipid peroxidation was evaluated on liver, brain and kidney homogenates, measuring both steady-state concentrations of thiobarbituric acid reactive substances, and fluorescent chromolipids, evaluated as hydroxynonenal adducts. Formation of thiobarbituric acid reactive substances was significantly higher in hyperglycemic than in normoglycemic animals. Three hours (but not 1 h) dehydroepiandrosterone-pretreatment protected tissues against lipid peroxidation induced by dextrose; both thiobarbituric acid reactive substances and hydroxynonenal adducts in liver, kidney and brain homogenates were significantly lower in dehydroepiandrosterone-pretreated animals. Dehydroepiandrosterone did not modify the cytosolic level of antioxidants, such as alpha-tocopherol or glutathione, nor the activities of glutathione peroxidase, reductase or transferase. The results of this study indicate that the 'in vivo' administration of dehydroepiandrosterone increases tissue resistance to lipid peroxidation triggered by acute hyperglycemia.

Mécanisme moléculaire de l'effet protecteur de la vitamine E dans l'athérosclérose

2002 ◽  
Vol 80 (7) ◽  
pp. 662-669 ◽  
Author(s):  
Abdelouahed Khalil
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Vascular Diseases ◽  
Epidemiologic Studies ◽  
Low Density Lipoproteins ◽  
Alpha Tocopherol ◽  
Low Density ◽  
Prooxidant Effect

Oxidation of low-density lipoproteins constitutes the first step of a very complex process leading to atherosclerosis. Vitamin E, and principally alpha-tocopherol, is considered as the principal inhibitor of lipid peroxidation. Some studies showed the beneficial role of vitamin E in the prevention and reduction of atherosclerosis and its associated pathologies. However, other in vitro studies advance a prooxidant role of vitamin E. The results of the epidemiologic studies are difficult to generalize without taking account of the clinical randomized tests. In this work, we reviewed the principal studies devoted to the role of vitamin E and discussed the assumption of a prooxidant effect of this molecule.Key words: vitamin E, low-density lipoproteins (LDL), lipid peroxidation, cardio-vascular diseases.

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