Protective Effect Of Α-tocopherol Research Articles

Involvement of lipid peroxidation in free fatty acid-induced isolated rat pancreatic acinar cell injury.

It was reported that free fatty acids degraded from triglycerides by lipase may play a major role in acute necrotizing or hyperlipidemia-induced pancreatitis. We hypothesized that this injury may be related to the peroxidation of cell membrane phospholipids and tested this hypothesis using isolated pancreatic acini. Pancreatic acini were prepared from male Sprague-Dawley rats by collagenase digestion. Linoleic acid was added (0.1-1.0 mM) to the acinar cell suspension to induce cell injury. Acinar cell damage was measured by lactate dehydrogenase release and by trypan blue exclusion. Phosphatidylcholine hydroperoxide and alpha-tocopherol in the acinar cells were measured. Protective effects of alpha-tocopherol (0.5, 5.0 mM) against this type of cell injury were also evaluated. When isolated acinar cells were treated with linoleic acid, a significant decrease in viability was observed in a time- and dose-dependent manner. In addition, the levels of phosphatidylcholine hydroperoxide after treatment of 0.5 mM of linoleic acid were increased and levels of alpha-tocopherol were decreased significantly. alpha-Tocopherol significantly ameliorated both cellular injury (p < 0.01) and increases in phosphatidylcholine hydroperoxide (p < 0.01). These data suggest that lipid peroxidation of the cellular membrane is an important component of the pancreatic cell injury mediated by free fatty acids.

Time-Level Relationship for Lipid Peroxidation and the Protective Effect of α-Tocopherol in Experimental Mild and Severe Brain Injury

Time-Level Relationship for Lipid Peroxidation and the Protective Effect of α-Tocopherol in Experimental Mild and Severe Brain Injury

Time-Level Relationship for Lipid Peroxidation and the Protective Effect of α-Tocopherol in Experimental Mild and Severe Brain Injury

Time-Level Relationship for Lipid Peroxidation and the Protective Effect of α-Tocopherol in Experimental Mild and Severe Brain Injury

Oxidative Changes Associated with β-Carotene and α-Tocopherol Enrichment of Human Low-Density Lipoproteins

Objective: To determine what effects enrichment of human low-density lipoprotein (LDL) with combinations of α-tocopherol and β-carotene would exert on LDL oxidation and attempt to define the nature of the effects.Methods: Human plasma was pooled and α-tocopherol and β-carotene was added in a four-by-four design resulting in the enrichment of LDL with α-tocopherol and β-carotene in varying concentrations. Enriched and control LDL was oxidized in Cu2+ mediated oxidation system and resistance of LDL to oxidation was determined by lag time, thiobarbituric acid reactive substances (TBARS) activity, and rate of oxidation.Results: Increasing LDL α-tocopherol concentration had a linear relationship with lag time and a negative correlation with rate of oxidation. LDL β-carotene concentration was linearly correlated with the rate of LDL oxidation and β-carotene loss, and exponentially related to TBARS concentration.Conclusions: These results support earlier findings for the protective effect of α-tocopherol against LDL oxidation, and suggest that β-carotene participates as a prooxidant in the oxidative degradation of LDL under these conditions. Since high levels of α-tocopherol did not mitigate the prooxidative effect of β-carotene, these result indicate that increased LDL β-carotene may cancel the protective qualities of α-tocopherol.

Lipid peroxidation: a novel enzymatic mechanism of protective effect of α-tocopherol in biological membranes.

Lipid peroxidation: a novel enzymatic mechanism of protective effect of α-tocopherol in biological membranes.

Protective effect of α-tocopherol on brain cell membrane function during cerebral cortical hypoxia in newborn piglets

Protective effect of α-tocopherol on the structure and function of brain cell membranes was investigated by measuring Na +,K +-ATPase activity and products of lipid peroxidation (fluorescent compounds) in brain cell membranes obtained from newborn piglets. Four groups of anesthetized, ventilated piglets were studied: five hypoxic piglets and five normoxic piglets were pretreated with free α-tocopherol (20 mg/kg/dose i.m.), five additional hypoxic piglets received i.m. placebo and five normoxic piglets served as control. Placebo and α-tocopherol were given 48 and 3 h prior to onset of hypoxia. Hypoxic hypoxia was induced and cerebral hypoxia was documented as a decrease in the ratio of phosphocreatine to inorganic phosphate (PCr/P i) using 31P NMR spectroscopy. PCR/P i decreased from baseline of2.62 ± 0.54to1.05 ± 0.27 in α-tocopherol-pretreated and from2.44 ± 0.48to1.14 ± 0.30 in the placebo-pretreated group during hypoxia. Na +,K +-ATPase activity was unchanged in both normoxic and hypoxic α-tocopherol-pretreated groups. However, in placebo-pretreated hypoxic group, Na +,K +-ATPase activity decreased as compared with control(44.9 ± 9.7vs.61.8 ± 5.7 μmol P i/mg protein/h, P < 0.005). The level of fluorescent compounds increased in placebo-pretreated but not in α-tocopherol-preatreated group as compared with control. During hypoxia, serum α-tocopherol levels were higher in α-tocopherol-pretreated groups as compared with placebo-pretreated hypoxic group. The present data indicates that α-tocopherol protects brain cell membranes in newborn piglets from lipid peroxidative damage during tissue hypoxia probably by being incorporated in cell membrane and also as circulating antioxidant.

Protective effect of α-tocopherol, ascorbic acid and rutin against peroxidative stress induced by oxidized lipoproteins on lymphoid cell lines

A new experimental model system consisting of lymphoid cell lines cultured in the presence of UV-treated low density lipoproteins (LDL) has been recently designed to investigate the cytotoxic effects of lipid peroxides entering the cell through the endocytotic pathway. We have compared the protective activities of several antioxidants, used alone or in combination

Protective effect of α-tocopherol on ischemic neuronal damage in the gerbil hippocampus

The effect of α-tocopherol (vitamin E) on ischemic neuronal damage was studied in the gerbil. The animals were subjected to 5 min of cerebral ichemia by bilateral common carotid artery occlusion. Immediately after ischemia, α-tocopherol at a dose of 50 or 100 mg/kg was administered intravenously. Morphological changes in the CA1 sector of the hippocampus were evaluated after 7 days of survival. α-Tocopherol prevented ischemia-induced neuronal death. The average density of CA1 pyramidal neurons (cells/mm, mean ± S.E.M.) was 252 ± 8 ( n = 8) in the sham-operated group, 50 ± 20 ( n = 8) in the ischemia group, and 140 ± 35 n = 8) and 182 ± 36 ( n = 8) in the groups treated with α-tocopherol at the doses of 50 and 100 mg/kg, respectively. The results suggest that free radical scavenging action of α-tocopherol played an important role in preventing the neuronal death.

Influence of α-tocopherol on prostacyclin synthesis by rat's arterial and myometrial tissues

Influence of α-tocopherol on PGI 2 synthesis by rat arterial and myometrial tissues was investigated using a rat platelet antiaggregatory bioassay. Chronic administration of α-tocopherol to female rats (10 mg kg −1 day −1 s.c. for 14 days) significantly increased ex-vivo PGI 2 synthesis by the arterial tissue from 12.7 ± 0.3 (control, mean ± s.e.m) to 17.2 ± 0.4 ng PGI 2 mg −1 wet tissue and by the myometrial tissue (in proestrus) from 1.1 ± 0.07 (control) to 1.85 ± 0.1 ng PGI 2 mg −1 wet tissue (P < 0.05, n = 6). α-tocopherol (5 mg kg −1day −1 for 14 days) did not stimulate PGI 2 to any significant level. Pretreatment of male rat arterial tissue with α-tocopherol (0.02, 0.1 or 0.2 mM) in vitro increased PGI 2 synthesis in a dose-dependent manner. At a dose of 0.2 mM it increased PGI 2 synthesis from 13.70 ± 0.70 (control) to 22.6 ± 1.4 ng PGI 2 mg −1 wet tissue (P < 0.1, n = 6). Pre-treatment of 14-day pregnant rat myometrium with α-tocopherol 0.2 and 0.4 mM significantly increased PGI 2 synthesis from 1.2 ± 0.06 (control) to 1.90 ± 0.12 and 2.1 ± 0.1 ng PGI 2 mg −1 wet tissue, respectively (P < 0.05, n = 6). The results indicate that the ability of α-tocopherol to stimulate PGI 2 synthesis may partly contribute towards better understanding of the mechanisms that underly the protective effect of α-tocopherol against experimentally induced decreases in coronary flow and intravascular coagulations in some mammals. Furthermore adequate intake of α-tocopherol during pregnancy may enhance uterine blood flow and ensure adequate foetal nutrition.

Protective effect of alpha-tocopherol on the morphological and rheological changes of rat red cells.

The effect of alpha-tocopherol on the rheological properties of rat red cells was studied. The suspension viscosity of red cells increased, as the alpha-tocopherol content in red cells decreased. The red cells gradually transformed to echinocytes in isotonic solution dependent on the alpha-tocopherol content. The unique correlations among the viscosity, the transformation, and alpha-tocopherol content were observed. It was shown that the increased suspension viscosity of alpha-tocopherol-deficient cells could have arisen from the difficulty of echinocytes to undergo high shear deformation. The possible mechanism is discussed.

Protective effect of α-tocopherol on cardiac muscle function during hypoxia and after reoxygenation

Protective effect of α-tocopherol on cardiac muscle function during hypoxia and after reoxygenation

ブリ筋肉のアクトミオシンの溶解度におよぼすレシチンの効果

1. Effect of added lecithin on the solubility of actomyosin during storage at 2°C was investigated. The decrease in the amount of soluble protein was protected proportionally with the amount of added leicthin. However, the protective effect became weaker with the progress of storage time, exhibiting the increase of TBA value in the actomyosin-lecithin system. 2. By the addition of α-tocopherol to the actomyosin-lecithin system, the increase of TBA value was diminished remarkably. Moreover, the protective effect of α-tocopherol on the decrease of soluble protein was enhanced with the duration of storage. 3. From these results, the possibility was discussed that the lecithin in reducing form would contribute to keeping the actomyosin in stable state.