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首页> 外文期刊>European journal of nutrition >Chronic vitamin E inadequacy and thermally treated oils affect the synthesis of hepatic metallothionein isoforms
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Chronic vitamin E inadequacy and thermally treated oils affect the synthesis of hepatic metallothionein isoforms

机译：慢性维生素E不足和热处理油会影响肝金属硫蛋白同工型的合成

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Background: Metallothionein (MT)~# synthesis can be stimulated in many organs not only by various metals such as cadmium, zinc, and copper, but also by many nonmetallic compounds or experimental conditions such as oxidative stress. The latter lead to the hypothesis that MT is induced in response to free radicals formed in tissues and lipid peroxidation. Aims of the study; Whether the relationship between lipid peroxidation and MT synthesis is a common phenomenon also valid for lipid peroxidation induced by dietary factors such as chronic vitamin E inadequacy and autoxidation products of polyenoic fatty acids derived from thermally oxiedized oil was investigated in the present study. Methods: The relationship between the induction of metallothionein isoforms I and II (MT-I and MT-II) in response to diet-induced lipid peroxidation using a rat model system in which lipid peroxidation was examined in vivo by chronic vitamin E inadequacy or by administration of lipid peroxidation products from a thermally treated polyenoicrich oil with either basal (dietary zinc concentration: 48 mg/kg; experiment 1) or Zn-stimulated MT levels (di-etary zinc concentration: 305 mg/kg; experiment 2) was studied. In both experiments. growing male rats were fed diets containing either a fresh or a thermally treated soybean oil with deficient or sufficient amounts of vitamin E (14 and 11 vs. 648 and 560mg #alpha#-tocopherol equivalents per kg diet) over 40 days according to a bifactorial experimental design. Plasma and liver concentrations of tocopherols and hepatic levels of thiobarbituric acid-reactive sub-stances (TBARS) were measured by high performance liquid chromatoraphy. MT isoform concentrations in rat liver were isolated and quantified by ion-exchange high performance liquid chromatography and atomic absorption spectrometry. Results: Irrespective of the zinc Supply. rats receiving inadequate amounts of vitmain E with the diet had markedly lower plasma and liver concentrations of #alpha#-tocopherol and total tocopherols than vitamin E-sufficient rats. ANOVA also revealed an interaction between the diet factors vitamin E and oil on tocopherols in plasma and liver of rats from both ex-beriments. In experiment 1, where rats received normal amounts of dietary zinc, ingestion of the thermally treated oil impaired the tocopherol status compared to the treatment with the fresh oil, although this effect was only obvious in the vitamin E-defi-cient groups. In experiment 2, where rats received excessive amounts of zinc, the thermally treated oil did not contribute to a reduction of the tocpherol status in plasma and liver. In both experiments a significant increase in TBARS level, indicative of lipid peroxidation, was observed in the liver at chronic vitamin E inadequacy, but no effect of the oil was observed. Here, we show that the dietary treatments had some effects on the synthesis of liver metallothionein isoforms. In groups, receiving normal amounts of zinc. there was a significant interaction between the dietary treatments on the levels of MT-I and MT-II in liver. chronic vitamin E inaequacy which was accompanied by diminished tocopherol levels in liver induced the synthesis of MT-I and MT-II. when vitamin E inadequacy was combined with the ingestion of a thermally treated polyenooic acid-rich oil hepatic levels of MT-I and MT-II remained low. In experiment 2, where rats were fed the high zinc diet. vitamin E inadequacy caused an increase of hepatic MT-I level just as in experiment 1, although this MT stimulating effect was irrespective of the oil. For MT-II there was a 43% increase in the vitamin E-deficient group fed the fresh oil compared to all the other groups. although this effect was not statistically significant. The liver MT isoform response to stress was similar in rats with basal MT levels and Zn-induced liver MT levels. The failing effect of the thermally treated oil on MT levels which were stimulated by vitamin E deficiency in experim
机译：背景：金属硫蛋白（MT）〜＃的合成不仅可以通过多种金属（例如镉，锌和铜），还可以通过许多非金属化合物或实验条件（例如氧化应激）来刺激。后者导致一个假设，即MT是对组织中形成的自由基和脂质过氧化反应的诱导。研究目的;在本研究中，研究了脂质过氧化与MT合成之间的关系是否是常见现象，对于是否由饮食因素（例如，长期维生素E不足和热氧化油衍生的多烯脂肪酸的自氧化产物）诱导的脂质过氧化也有效。方法：使用大鼠模型系统对饮食引起的脂质过氧化反应中金属硫蛋白同工型I和II（MT-I和MT-II）的诱导之间的关系，该模型系统通过体内慢性维生素E不足或通过体内脂质过氧化检查研究了热处理后的多烯富油的脂质过氧化产物的添加量（基础（膳食锌浓度：48 mg / kg;实验1）或锌刺激的MT水平（膳食锌浓度：305 mg / kg;实验2）） 。在两个实验中。根据双因素分析，在40天内，向生长中的雄性大鼠饲喂含有新鲜或热处理大豆油且维生素E不足或充足的饮食（14和11与648和560mg＃alpha＃-生育酚当量/ kg饮食）实验设计。通过高效液相色谱法测定血浆和肝脏中生育酚的浓度以及肝脏中硫代巴比妥酸反应性物质（TBARS）的水平。通过离子交换高效液相色谱和原子吸收光谱法分离和定量大鼠肝脏中的MT同工型浓度。结果：与锌供应无关。与维生素E充足的大鼠相比，饮食中摄入的维生素E含量不足的大鼠的血浆和肝脏中的＃alpha＃-生育酚和总生育酚的浓度显着降低。方差分析还揭示了饮食因素中的维生素E和油脂对两种前驱大鼠血浆和肝脏中生育酚的相互作用。在实验1中，大鼠接受正常量的饮食锌，与新鲜油相比，摄入经热处理的油会损害生育酚的状态，尽管这种作用仅在缺乏维生素E的人群中很明显。在实验2中，老鼠接受了过量的锌，热处理过的油不会降低血浆和肝脏中的生育酚状态。在两个实验中，在慢性维生素E不足的情况下，在肝脏中均观察到表明脂质过氧化的TBARS水平显着增加，但未观察到该油的作用。在这里，我们表明饮食治疗对肝脏金属硫蛋白同工型的合成有一些影响。分组接受正常量的锌。在肝脏中，MT-1和MT-2的饮食治疗之间存在显着的相互作用。慢性维生素E不足并伴有肝脏中的生育酚水平降低，诱导了MT-I和MT-II的合成。当维生素E不足与经热处理的富含多烯酸的油的摄入相结合时，MT-I和MT-II的肝水平仍然很低。在实验2中，给老鼠喂了高锌饮食。维生素E的不足会导致肝脏MT-1水平升高，与实验1一样，尽管这种MT刺激作用与油脂无关。对于MT-II，与所有其他组相比，补充新鲜油的维生素E缺乏组增加了43％。尽管这种效果在统计学上不显着。在基础MT水平和锌诱导的肝MT水平的大鼠中，肝MT同工型对应激的反应相似。维生素E缺乏刺激的热处理油对MT水平的失效作用

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