Rat lung microsomal lipid peroxidation: effects of vitamin E and reduced glutathione

1986 ◽  
Vol 61 (2) ◽  
pp. 785-790 ◽  
Author(s):  
D. P. Franco ◽  
S. G. Jenkinson
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Liver Microsomes ◽  
Sulfhydryl Group ◽  
Rat Lung ◽  
Active Components ◽  
Microsomal Lipid Peroxidation ◽  
Microsomal Membranes ◽  
High Concentrations

Lung microsomal membranes that contain the redox active components associated with the mixed-function oxidase system can be peroxidized in vitro. To investigate the characteristics of rat lung microsomal lipid peroxidation, we performed experiments using a variety of peroxidation initiators and microsomes obtained from normal and vitamin E-deficient rats. We found that lung microsomes obtained from normal rats are peroxidized much less than liver microsomes obtained from the same animals. Only initiation systems using very high concentrations of ferrous iron produced any significant peroxidation of normal rat lung microsomes. Lung microsomes obtained from vitamin E-deficient rats were found to be much more susceptible to peroxidation. Glutathione (GSH) was effective in inhibiting peroxidation when lung microsomes from normal rats were peroxidized. GSH was not effective in decreasing peroxidation when microsomes from vitamin E-deficient rats were peroxidized in the same system. We conclude that both GSH and vitamin E protect lung microsomal membranes from peroxidation. Glutathione protection appears to be related to the presence of a sulfhydryl group.

scholarly journals Inhibition of microsomal lipid peroxidation by glutathione and glutathione transferases B and AA. Role of endogenous phospholipase A2

1984 ◽  
Vol 220 (1) ◽  
pp. 243-252 ◽  
Author(s):  
K H Tan ◽  
D J Meyer ◽  
J Belin ◽  
B Ketterer
Keyword(s):  
Lipid Peroxidation ◽  
Phospholipase A2 ◽  
Rat Liver ◽  
Inhibitory Activity ◽  
Liver Microsomes ◽  
Supernatant Fraction ◽  
Rat Liver Microsomes ◽  
Microsomal Lipid Peroxidation ◽  
Soluble Supernatant

Lipid peroxidation in vitro in rat liver microsomes (microsomal fractions) initiated by ADP-Fe3+ and NADPH was inhibited by the rat liver soluble supernatant fraction. When this fraction was subjected to frontal-elution chromatography, most, if not all, of its inhibitory activity could be accounted for by the combined effects of two fractions, one containing Se-dependent glutathione (GSH) peroxidase activity and the other the GSH transferases. In the latter fraction, GSH transferases B and AA, but not GSH transferases A and C, possessed inhibitory activity. GSH transferase B replaced the soluble supernatant fraction as an effective inhibitor of lipid peroxidation in vitro. If the microsomes were pretreated with the phospholipase A2 inhibitor p-bromophenacyl bromide, neither the soluble supernatant fraction nor GSH transferase B inhibited lipid peroxidation in vitro. Similarly, if all microsomal enzymes were heat-inactivated and lipid peroxidation was initiated with FeCl3/sodium ascorbate neither the soluble supernatant fraction nor GSH transferase B caused inhibition, but in both cases inhibition could be restored by the addition of porcine pancreatic phospholipase A2 to the incubation. It is concluded that the inhibition of microsomal lipid peroxidation in vitro requires the consecutive action of phospholipase A2, which releases fatty acyl hydroperoxides from peroxidized phospholipids, and GSH peroxidases, which reduce them. The GSH peroxidases involved are the Se-dependent GSH peroxidase and the Se-independent GSH peroxidases GSH transferases B and AA.

scholarly journals Evaluation of α-tocopherol antioxidant activity in microsomal lipid peroxidation as detected by low-level chemiluminescence

1984 ◽  
Vol 223 (3) ◽  
pp. 755-759 ◽  
Author(s):  
E Cadenas ◽  
M Ginsberg ◽  
U Rabe ◽  
H Sies
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Induction Period ◽  
Chemiluminescence Intensity ◽  
Low Level ◽  
Naturally Occurring ◽  
Microsomal Lipid Peroxidation ◽  
Microsomal Membranes ◽  
And Control ◽  
Free Radical Process

The significance of microsomal vitamin E in protecting against the free-radical process of lipid peroxidation was evaluated with the low-level-chemiluminescence technique in microsomal fractions from vitamin E-deficient and control rats. The induction period that normally precedes the ascorbate/ADP/Fe3+-induced lipid peroxidation was taken as reflecting the microsomal vitamin E content and was found to be 5-6-fold decreased in microsomal fractions from vitamin E-deficient rats. Supplementation of microsomal fractions from vitamin E-deficient rats with exogenous vitamin E partially restores the induction period observed in that from control rats. The decrease in chemiluminescence intensity and the increase in the induction period both correlate linearly with the amount of vitamin E added. However, the efficiency of exogenous vitamin E is about 50-fold lower than that exerted by the naturally occurring vitamin E in microsomal membranes. These observations are discussed in terms of the process of re-incorporation of vitamin E into membranes, the experimental model for lipid peroxidation selected, and the method to evaluate lipid peroxidation, namely low-level chemiluminescence.

Influence of vitamin E and nitrogen dioxide on lipid peroxidation in rat lung and liver microsomes

Lipids ◽  
1982 ◽  
Vol 17 (4) ◽  
pp. 269-277 ◽  
Author(s):  
Alex Sevanian ◽  
Allen D. Hacker ◽  
Nabil Elsayed
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Nitrogen Dioxide ◽  
Liver Microsomes ◽  
Rat Lung

scholarly journals Stimulation of lipid peroxidation and hydroxyl-radical generation by the contents of human atherosclerotic lesions

1992 ◽  
Vol 286 (3) ◽  
pp. 901-905 ◽  
Author(s):  
C Smith ◽  
M J Mitchinson ◽  
O I Aruoma ◽  
B Halliwell
Keyword(s):  
Lipid Peroxidation ◽  
Copper Ions ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Atherosclerotic Lesions ◽  
Arterial Lesions ◽  
Human Cadavers ◽  
Radical Generation ◽  
Almost All

Lipid peroxidation within human arterial lesions is thought to play an important role in the development of atherosclerosis. Peroxidation can be accelerated by the presence of ‘catalytic’ iron or copper ions. Gruel samples from advanced atherosclerotic lesions in the abdominal aortae of human cadavers were tested for pro-oxidant properties. All samples contained bleomycin-detectable iron and phenanthroline-detectable copper. Almost all gruel samples stimulated peroxidation of rat liver microsomes, and this was usually inhibited by the iron-ion chelator desferrioxamine. Some samples stimulated formation of hydroxyl radicals from H2O2 in the presence of ascorbate, a reaction again inhibited by desferrioxamine. We conclude that the interior of human advanced atherosclerotic lesions is a highly pro-oxidant environment, and that the use of copper or iron ions to promote peroxidation of low-density lipoproteins in vitro may be a valid model for events in the arterial wall.

The in vitro effect of Helichrysi flos on microsomal lipid peroxidation

2001 ◽  
Vol 77 (1) ◽  
pp. 31-35 ◽  
Author(s):  
E. Czinner ◽  
K. Hagymási ◽  
A. Blázovics ◽  
Á. Kéry ◽  
É. Szőke ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Microsomal Lipid Peroxidation ◽  
Vitro Effect

Vitamin E Reduces Monocyte Tissue Factor Expression in Cirrhotic Patients

Blood ◽  
1999 ◽  
Vol 93 (9) ◽  
pp. 2945-2950 ◽  
Author(s):  
Domenico Ferro ◽  
Stefania Basili ◽  
Domenico Praticó ◽  
Luigi Iuliano ◽  
Garret A. FitzGerald ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Liver Cirrhosis ◽  
Vitamin E ◽  
Tissue Factor ◽  
Standard Therapy ◽  
Pathophysiological Mechanism ◽  
Important Mediator ◽  
Factor Expression ◽  
Cirrhotic Patients

Clotting activation may occur in liver cirrhosis, but the pathophysiological mechanism has not been fully elucidated. Because a previous study demonstrated that lipid peroxidation is increased in cirrhosis, we analyzed whether there is a relationship between lipid peroxidation and clotting activation. Thirty cirrhotic patients (19 men and 11 women; age, 34 to 79 years) and 30 controls matched for sex and age were investigated. In all subjects, monocyte expression of tissue factor (TF) antigen and activity; plasma levels of prothrombin fragment 1+2 (F1+2), a marker of thrombin generation; and urinary excretion of Isoprostane-F2-III, a marker of lipid peroxidation, were measured. Furthermore, the above-reported variables were re-evaluated after 30 days of treatment with standard therapy (n = 5) or standard therapy plus 300 mg vitamin E twice daily (n = 9). In addition, we analyzed in vitro if vitamin E (50 μmol/L) influenced monocyte TF expression and F1+2 generation. Cirrhotic patients had higher values of Isoprostane-F2-III (P < .0001), F1+2 (P < .0001), and monocyte TF antigen (P < .0001) and activity (P < .03) than controls. Isoprostane-F2-III was significantly correlated with F1+2 (Rho = 0.85; P < .0001) and TF antigen (Rho = 0.95; P < .0001) and activity (Rho = 0.94;P < .0001). After vitamin E treatment, Isoprostane-F2-III (P = .008), F1+2 (P < .008), and monocyte TF antigen (P = .012) and activity (P = .008) significantly decreased; no changes of these variables were detected in patients not receiving vitamin E. In vitro, vitamin E significantly reduced the expression of monocyte TF antigen (−52%; P = .001) and activity (−55%; P= .003), as well as F1+2 generation (−51%; P = .025). This study shows that vitamin E reduces both lipid peroxidation and clotting activation and suggests that lipid peroxidation may be an important mediator of clotting activation in liver cirrhosis.

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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