Vitamin E-Supplemented Diets Reduce Lipid Peroxidation but Do Not Alter Either Pituitary-Adrenal, Glucose, and Lactate Responses to Immobilization Stress or Gastric Ulceration

It has been suggested that antioxidant administration to rats would reduce the physiological response to stress. In the present experiment adult male rats were given diets supplemented with vitamin E for one or seven days before they were subjected to immobilization stress. Vitamin E administration reduced hepatic and gastric lipid peroxidation in unstressed rats but did not modify the pituitary-adrenal, glucose and lactose responses to I or 18 h immobilization. Similarly, gastric ulceration caused by 18 h immobilization was unaffected by the diets. These results indicate that the inhibition of lipid peroxidation does not modify the response of several, well-known, stress-markers in the rat.     

Effects of Vitamin A and Its Analogs on Nonenzymatic Lipid Peroxidation in Rat Brain Mitochondria

Vitamin A (retinol) and some of its analogs exhibited varying degrees of inhibition on induced iron and ascorbic acid lipid peroxidation of rat brain mitochondria. Malonyldialdehyde production was used as an index of the extent of in vitro lipid peroxidation. The fat-soluble vitamins retinol, retinol acetate, retinoic acid, retinol palmitate, and retinal at concentrations between 0.1 and 10.0 mmol/L inhibited brain lipid peroxidation. Retinol and retinol acetate were the most effective inhibitors. It is concluded from this study that retinol and its analogs can be considered as potential antioxidant factors, more potent than some of the well-known antioxidants such as alpha-tocopherol and butylated hydroxytoluene.     

Blood plasma levels of lipoperoxides,glutathione peroxidase,beta carotene,vitamin A and E in women with habitual abortion

The plasma levels of lipoperoxides, glutathione peroxidase (GSH-Px), reduced glutathione (GSH), beta carotene, vitamin A, E, some plasma biochemical and blood haematological parameters were investigated in 40 women with habitual abortion (HA) and controls. The levels of GSH, vitamin A, E and beta carotene were significantly lower in women with HA than in controls. However, the plasma levels of lipid peroxidation, alkaline phosphatase (ALP), glucose and blood haemoglobin were significantly higher in HA than in controls. In addition, plasma levels of GSH-Px, AST, ALT, total bilirubin, total protein, albumin, sodium, potassium, calcium and number of white blood cells, red blood cells, platelet and values of packet cell volume showed no significant differences between HA and controls. According to the results of this study, we observed that the levels of lipid peroxidation were increased and plasma levels of vitamin A, E and beta carotene were decreased in HA. The decrease of those antioxidants may play a significant role in women with habitual abortion. Copyright © 1998 John Wiley & Sons, Ltd.     

硝普纳处理对白刺愈伤组织膜脂过氧化及抗氧化酶活性的影响

以唐古特白刺（Nitraria tangutorum Bobr.）愈伤组织为材料,研究一氧化氮(NO)供体硝普钠（SNP）处理对其膜脂过氧化及抗氧化酶活性的影响。激光共聚焦扫描显微镜技术检测结果显示,白刺愈伤组织在SNP处理下细胞中NO含量显著增加,而N-硝基-L-精氨酸（L-NNA）处理使细胞中NO水平降低。低浓度SNP（10和25 μmol·L^-1）处理后,白刺愈伤组织中丙二醛（MDA）含量显著减少,而高浓度SNP（100 μmol·L^-1）和L-NNA(0.5 mmol·L^-1)处理后MDA含量明显高于对照。与对照比,SNP处理诱导白刺愈伤组织可溶性蛋白含量升高,却使脯氨酸含量减少。白刺愈伤组织在不同浓度SNP处理下过氧化氢酶（CAT）和抗坏血酸过氧化物酶（APX）活性呈增加的变化趋势,低浓度SNP处理使过氧化物酶（POD）活性减弱,而50 μmol·L^-1 SNP处理后POD活性约增加为对照的119%。结果提示,外源NO可促进白刺愈伤组织可溶性蛋白的合成,诱导抗氧化酶活性升高,增强了白刺愈伤组织的抗氧化能力,从而表现出对细胞的保护作用。     

Effect of Bilirubin on Lipid Peroxidation, Sphingomyelinase Activity, and Apoptosis Induced by Sphingosine and UV Irradiation

The effect of bilirubin (BR) on sphingomyelin cycle activity, lipid peroxidation (LPO), and apoptosis induced by sphingosine and UV irradiation has been studied in vivo. Neutral Mg²⁺-dependent sphingomyelinase (SMase) activity and LPO level were monitored in heart, kidney, and liver of mice after administration of BR. BR inhibited both LPO and SMase activities in heart and kidney. BR induced a mild increase in LPO level and moderate increase in lipid contents in liver, consistent with the functional role of liver in both BR and lipid metabolism. BR injected to mice causes simultaneous and unidirectional alterations in both LPO level and SMase activity with a significant (p < 0.05) positive linear correlation between these two parameters. Sphingosine administration results in increased lipid peroxidation in murine liver. Data on DNA fragmentation indicate that exogenous BR may effectively protect thymus cells against sphingosine- and UV-mediated apoptosis. These results have revealed a biochemical association between oxidative stress and BR on one hand and the sphingomyelin cycle and apoptotic cell death on the other hand. Our data show that BR as an antioxidant, due to its effect on the sphingomyelin cycle, can protect membrane lipids against peroxidation and cells against apoptosis induced by various factors.     

Antioxidant effect of vitamin E and glutathione on lipid peroxidation in boar semen plasma

The protective effect of vitamin E and reduced glutathione (GSH) against lipid peroxidation in boar semen plasma was studied. The lipid peroxidation, measured by the test for thiobarbituric acid reactive substances (TBARS), doubled in the presence of the lipid peroxidation Fe²⁺-sodium ascorbate-inducing system. The ascorbate-induced TBARS were inhibited by about 62% through the water-soluble vitamin E analog (TROLOX) and about 57% by GSH. In the in vivo experiments, 7 wk of oraldl-α-tocopherol acetate (1000 IU/d/animal) administration caused a significant fall in the level of the semen plasma TBARS, from 2.2±0.09 to 1.2±0.13 nmol MDA/mL. The semen plasma superoxide dismutase (SOD) and GSSG tended to increase with the time of vitamin E administration, but the increment did not reach a significant level by the seventh week. The vitamin E supplementation significantly increased the number of spermatozoa per 1 cm³ of ejaculate. The protective role of vitamin E and GSH with respect to boar semen against fatty acid peroxidation and a positive influence of vitamin E supplementation on semen quality have been evidenced.     

The Effect of Vitamin E-Deficiency in Isolated Rat Heart on the Cellular Defence System Against Free Radicals During Normal Reperfusion After Hypoxic, Ischemic and Ca2+-Free Perfusion

We investigated whether vitamin E plays a role in the protection against potential free radical formation and related biochemical changes in hypoxic, ischemic and Ca²⁺-depleted rat heart upon normal reperfusion.

In the heart of normally fed rats a decrease in the activity of superoxide dismutase and the capacity of the glutathione system, factors of the cellular protective mechanisms against free radicals, occurred upon exposure to the above mentioned treatments. This decrease was not further enhanced if vitamin E-deficient rat hearts were treated. Vitamin E-deficiency, however, led to detectable peroxidation of lipids if Ca²⁺-depleted or hypoxic hearts were reperfused. Lipid peroxidation was measured as the formation of thiobarbituric acid reactive material, which is readily formed during this process. Reflow after ischemia did not induce lipid peroxidation either in normal or in vitamin E-deficient rat heart.

Since changes in Ca²⁺ -homeostasis are thought to be primarily responsible for the Ca²⁺-reperfusion injury, a role for Ca²⁺-ions in lipid peroxidative processes, either directly or indirectly, seems indicated. Furthermore the results imply that even a sharp and extensive decrease of reduced glutathione, as seen upon Ca²⁺ -repletion after a period of Ca²⁺ -depletion, does not necessarily induce peroxidation of lipids in heart tissue. Obviously, vitamin E is very important in the protection of cardiac membranes. Replenishment of the water-soluble protective factors in the heart seems, however, more important during above mentioned treatments, especially since repair of the vitamin E-free radical is dependent on water-soluble factors.     

Influence of dietary vitamin E (DL-alpha-tocopheryl acetate) and diludine (diethyl 1,4-dihydro-2,6-dimethyl-3,5-pyridinedicarboxylate) levels on growth and lipid peroxidation in rainbow trout,Oncorhynchus mykiss

We aimed to investigate the influence of dietary vitamin E and diludine on growth and lipid peroxidation (malondialdehyde; MDA) in rainbow trout. Fish (1.5 g) were fed different dietary levels of vitamin E (0, 50 and 100 mg/kg) and diludine (0, 0.5 and 1 g/kg) for 10 weeks. Growth performance and feed conversion ratio (FCR) were significantly affected by dietary vitamin E (p < .05) but not diludine. Fish fed 50 mg/kg dietary vitamin E with no diludine had significantly better growth and lower FCR than those fed vitamin E free diets. Liver vitamin E content was significantly influenced by dietary vitamin E and diludine (p < .05). The highest hepatic vitamin E was in fish fed the highest dietary vitamin E and diludine levels. Hepatic MDA level was significantly affected by dietary vitamin E and diludine (p < .05), decreasing with the increase in both dietary vitamin E and diludine. According to our results, diludine had no significant effect on growth; however, decreased hepatic lipid peroxidation independent of vitamin E. Our results reveal that 50 mg/kg vitamin E content is suitable for optimal growth and FCR in rainbow trout juveniles. However, dose dependent effects of dietary diludine remain uncertain and need further researches.     

Effect of Vitamin E and Its Analogues Having Various Molecular Structures on the Growth and Lipid Composition of Pythium debaryanum

The effect of exogenously added vitamin E and its synthetic analogues (the hydrophilic form of vitamin E and chromans C₁₃and C₁) at a concentration of 9.86 × 10^–5M on the growth, lipogenic activity, and the fatty acid composition of the eicosapolyenoic acid–synthesizing oomycete Pythium debaryanumwas studied. The effect was found to depend on the molecular structure of particular compounds. For instance, vitamin E and chroman C₁₃stimulated fungal growth, whereas chroman C₁inhibited it. The hydrophilic form of vitamin E enhanced the lipogenic activity of the oomycete. The studied compounds, which possess antioxidant activity, did not exert any noticeable effect on the content of eicosapolyenoic acids and the degree of the unsaturation of fungal lipids.     

Effect of Toluene and Nutritional Status on Serotonin,Lipid Peroxidation Levels and NA<Superscript>+</Superscript>/K<Superscript>+</Superscript>-ATPase in Adult Rat Brain

The aim was to evaluate the effect of toluene and nutritional status on levels of serotonin (5-HT), 5-hydroxytryptophan (5-HTP), Na⁺/K⁺-ATPase, total ATPase and lipid peroxidation (TBARS) in rat brain. Study was conducted with malnourished (MN), well-nourished (WN) and normal Wistar rats. Three groups were formed for each nutritional status: control group I received 0.9% NaCl; toluene (1 g/kg) was administered to group II, and 1.5 g/kg to group III. Levels of 5-HT decreased (P < 0.05) in WN toluene groups, and 5-HTP decreased (P < 0.05) in the WN 1 g toluene and MN 1.5 g toluene groups. TBARS decreased (P < 0.05) in WN toluene groups. A trend to increase in Na⁺/K⁺-ATPase was found in WN and MN toluene groups, while total ATPase increased (P < 0.05) in the WN 1.5 g toluene group. The results suggest that high concentrations of toluene in single doses induce significant changes in the serotonergic system and alter membrane fluidity more perceptibly in the brain of adult animals with regular diet than in malnourished animals.