scholarly journals Brain Lipid Peroxidation Induced by Postischemic Reoxygenation in vitro: Effect of Vitamin E

1984 ◽  
Vol 4 (3) ◽  
pp. 466-469 ◽  
Author(s):  
Shinichi Yoshida ◽  
Raul Busto ◽  
Mercedes Santiso ◽  
Myron D. Ginsberg
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Lipid Peroxides ◽  
Aerobic Incubation ◽  
Ischemic Hypoxia ◽  
Brain Lipid Peroxidation ◽  
Vitro Effect ◽  
The Brain ◽  
Slow Propagation

The aerobic incubation of brain afer a period of ischemia induced lipid peroxidation. The effect was greatest in vitamin E—deficient rats, intermediate in vitamin E—normal rats, and least in animals supplemented with vitamin E. In contrast, nitrogen incubation following ischemia produced a small effect only in the vitamin E—deficient animals. It appears that reoxygenation is required for lipid peroxides to accumulate in the brain. However, a trace of oxygen remaining during extreme ischemic hypoxia may be sufficient to cause slow propagation of free radical reactions when the vitamin E level is low.

scholarly journals Vitamin E and hepatotoxic agents

1969 ◽  
Vol 23 (2) ◽  
pp. 297-307 ◽  
Author(s):  
J. Green ◽  
J. Bunyan ◽  
M. A. Cawthorne ◽  
A. T. Diplock
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Rat Liver ◽  
Protective Action ◽  
Lipid Peroxides ◽  
Ultraviolet Region ◽  
Intraperitoneal Dose ◽  
And Control

1. It has been suggested that carbon tetrachloride damages rat liver by accelerating processes of lipid peroxidation at subcellular sites and that the protective action of vitamin E is due to its functioning as an antioxidant in vivo. Direct evidence for these mechanisms in vivo has been sought and is critically examined.2. The increased production of malondialdehyde by rat liver microsomal fractions during incubation with CCl4 was shown to be a function of the vitamin E status of the rat and of an in vitro reaction, which could not be correlated with the hepatotoxic action of CCI4.3. Evidence for the production of lipid peroxides by CCl4 in the livers of vitamin E-deficient and vitamin E-supplemented rats was sought (I) by measurement of ultraviolet spectral changes ('diene' formation) and (2) by direct micro-iodimetric determination of the peroxide. No differences in peroxide content were found between CC14-treated and control rats, nor were the spectrophotometric changes in the ultraviolet region related to the presence of vitamin E.4. The effect of CCI4 (2.0 ml/kg orally) on ATP levels in rat liver was studied at intervals from 3 to 68 h. The primary lesion leading to necrosis and fat accumulation after CCl4 treatment occurred many hours before the eventual slight decline in ATP. Although the levels of ATP were somewhat higher in vitamin E-deficient rats, vitamin E did not prevent the slight decline in ATP that took place. Since ATP is known to be highly sensitive to peroxidation, the results suggest that lipid peroxidation is not the primary event in CCl4 poisoning.5. The effect of CC14on the metabolism of [14C]D-α-tocopherol in the rat was studied. A single intraperitoneal dose of CCl4 (2.0 m/kg) did not increase the destruction of α-tocopherol in the liver or carcass after 24 h. Three smaller daily doses of CC14 (0.25 ml/kg) also did not increase α-tocopherol catabolism; on the contrary, significantly more α-tocopherol was found in the livers of rats treated with CCI4. These results suggest that CCl4 does not increase lipid peroxidation in vivo.

scholarly journals Transplanted Oligodendrocyte Progenitor Cells Survive in the Brain of a Rat Neonatal White Matter Injury Model but Less Mature in Comparison with the Normal Brain

2020 ◽  
Vol 29 ◽  
pp. 096368972094609
Author(s):  
Shino Ogawa ◽  
Mutsumi Hagiwara ◽  
Sachiyo Misumi ◽  
Naoki Tajiri ◽  
Takeshi Shimizu ◽  
...  
Keyword(s):  
White Matter ◽  
Replacement Therapy ◽  
Fluorescent Protein ◽  
White Matter Injury ◽  
Normal Brain ◽  
Cell Replacement Therapy ◽  
Cell Replacement ◽  
Vitro Effect ◽  
The Brain

Preterm infants have a high risk of neonatal white matter injury (WMI) caused by hypoxia-ischemia. Cell-based therapies are promising strategies for neonatal WMI by providing trophic substances and replacing lost cells. Using a rat model of neonatal WMI in which oligodendrocyte progenitors (OPCs) are predominantly damaged, we investigated whether insulin-like growth factor 2 (IGF2) has trophic effects on OPCs in vitro and whether OPC transplantation has potential as a cell replacement therapy. Enhanced expression of Igf2 mRNA was first confirmed in the brain of P5 model rats by real-time polymerase chain reaction. Immunostaining for IGF2 and its receptor IGF2 R revealed that both proteins were co-expressed in OLIG2-positive and GFAP-positive cells in the corpus callosum (CC), indicating autocrine and paracrine effects of IGF2. To investigate the in vitro effect of IGF2 on OPCs, IGF2 (100 ng/ml) was added to the differentiation medium containing ciliary neurotrophic factor (10 ng/ml) and triiodothyronine (20 ng/ml), and IGF2 promoted the differentiation of OPCs into mature oligodendrocytes. We next transplanted rat-derived OPCs that express green fluorescent protein into the CC of neonatal WMI model rats without immunosuppression and investigated the survival of grafted cells for 8 weeks. Although many OPCs survived for at least 8 weeks, the number of mature oligodendrocytes was unexpectedly small in the CC of the model compared with that in the sham-operated control. These findings suggest that the mechanism in the brain that inhibits differentiation should be solved in cell replacement therapy for neonatal WMI as same as trophic support from IGF2.

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.

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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