The effects of vitamin A nutritional status on glutathione levels and microsomal lipid peroxidation in rat lung

Summary In vitamin A-deficient rats, the glutathione level in lung was diminished and microsomal lipid peroxidation much increased. In vitamin A-loaded animals, however, both were depressed below control. Thus vitamin A protection against lipid peroxidation is independent of glutathione.Acknowledgments. We thank Dr L. Y. Y. Fong and Mr David Y. H. Woo for preparing the animals used in this research, for retinol determinations and for valuable discussions, and also the China Medical Board of New York and the University of Hong Kong for the award of a Fellowship to V.P.     

The effects of vitamin A nutritional status on glutathione,glutathione transferase and glutathione peroxidase activities in rat intestine

Summary In rat intestine, the glutathione level was increased, glutathione peroxidase activity decreased and glutathione-S-transferase unchanged by vitamin A deficiency.     

Dietary vitamin E does not protect from endotoxin-induced hepatic microvascular dysfunction

Starting from the concept that lipopolysaccharide (LPS)-associated hepatotoxicity involves the action of reactive oxygen species, the present study was conducted to test whether vitamin E, a lipophilic antioxidant, prevents LPS-induced hepatic microvascular dysfunction and liver injury. Fifty-two rats were divided into three groups and fed diets containing 0 (n=16), 75 (n=18) or 8000 mg (n=18) α-tocopherol acetate/kg food for four weeks. At 1 h and 6 h after intravenous LPS-exposure (10 mg/kg E. coli LPS) hepatic microvascular response and liver injury were assessed by the analysis of Kupffer cell phagocytic activity, leukocyte-endothelial cell interaction and nutritive sinusoidal perfusion (intravital fluorescence epi- illumination technique) as well as bile flow, serum liver enzyme activities and tissue histomorphology. In animals fed with 75 mg vitamin E/kg (standard diet), LPS caused hepatic Kupffer cell activation (increased phagocytic activity) and hepatic microvascular leukocyte activation, with stasis in sinusoids and adherence in postsinusoidal venules (1 h) followed by leukocytic infiltration into tissue (6 h) and progredient sinusoidal perfusion failure (6 h). Hepatic microvascular injury was accompanied by reduced bile flow and enhanced liver enzyme release. Vitamin E-enriched diet (8000 mg/kg) and even vitamin E-deficient diet did not significantly affect LPS-induced hepatic microvascular cell activation and perfusion failure. Thus, we conclude, that vitamin E is not effective to protect from endotoxin-induced hepatic microvascular dysfunction. Received 7 November 1996; received after revision 30 December 1996; accepted 20 January 1997     

The effects of vitamin A nutritional status on glutathione levels and microsomal lipid peroxidation in rat lung

In vitamin A-deficient rats, the glutathione level in lung was diminished and microsomal lipid peroxidation much increased. In vitamin A-loaded animals, however, both were depressed below control. Thus vitamin A protection against lipid peroxidation is independent of glutathione.     

The effects of vitamin A nutritional status on microsomal lipid peroxidation and alpha-tocopherol level in rat liver

In vitamin A-deficient rats, liver glutathione peroxidase activity was decreased, alpha-tocopherol content was strongly enhanced, but microsomal liquid peroxidation remained unchanged.     

Effects of chronic caffeine feeding on the activities of oxygen free radical defense enzymes in the growing rat heart and liver

The purpose of the present study was to determine the relationship between concentration of Zn, Cu and Fe, and the catalase, glutathione peroxidase and superoxide dismutase activities in the heart and liver of newborn rats whose dams were fed a diet supplemented with caffeine. Heart Zn levels of the 22- and 30-day-old rats of the caffeine group showed a decrease, whereas liver Zn levels showed an increase compared to the control. Cu levels in the liver at day 22 in the caffeine group were less than in the control. Cu- and Zn-containing superoxide dismutase activities showed an increase in the hearts of the caffeine group compared to the control. The activity of catalase and glutathion peroxidase showed no difference in the heart and liver between the groups. The present study suggests the possible involvement of superoxide dismutase enzyme in the impairment of heart formation as a result of chronic caffeine intake in the early growing period.     

The effects of vitamin A nutritional status on glutathione, glutathione transferase and glutathione peroxidase activities in rat intestine

In rat intestine, the glutathione level was increased, glutathione peroxidase activity decreased and glutathione-S-transferase unchanged by vitamin A deficiency.     

氧化酪蛋白对小鼠组织抗氧化能力及血液肽组成的影响

目的研究酪蛋白经过加热氧化和脂质过氧化物MDA氧化后,对小鼠体内氧化还原状态及小鼠血液中肽组成的影响。方法酪蛋白经100℃加热（0、30、60、90min）和丙二醛（MDA）氧化（MDA终浓度0、0．2、20、200mmol／L）处理,测定其羰基、巯基含量及表面疏水性的变化。小鼠分为四组,分别灌胃生理盐水、正常酪蛋白、加热90rain、MDA氧化酪蛋白,测定0、30、60、90、120、160min血液中自由基水平,并采用HPLC-MS分析灌胃后120min小鼠血浆肽组分的变化,测定小鼠的肝脏、空肠、十二指肠组织抗氧化能力指标（总抗氧化能力T—AOC、丙二醛MDA、还原型谷胱甘肽GSH）。结果酪蛋白经过两种氧化处理,羰基含量均随氧化程度呈显著上升,巯基含量呈下降趋势。加热氧化后酪蛋白表面疏水性比正常酪蛋白低,而MDA氧化导致疏水性上升。小鼠血液中自由基最高峰出现在灌胃后160min。灌胃两种方式处理的酪蛋白,血液中自由基的含量均显著高于灌胃正常酪蛋白组（P〈0．05）,肝脏、空肠、十二指肠还原型谷胱甘肽（GSH）含量和总抗氧化能力（T-AOC）均低于正常酪蛋白组,丙二醛（MDA）含量显著提高（P〈0．05）。HPLC—MS分析显示,灌胃MDA氧化酪蛋白组血液中肽组成与对照组不同,出现c7H15N4O含羰基类的物质：结论氧化会导致酪蛋白理化性质的改变,摄入氧化酪蛋白引起机体的氧化应激,降低组织抗氧化能力。