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饮食中补充维生素E、核黄素和硒对中枢神经系统氧中毒的影响。

Effects of dietary supplementation with vitamin E, riboflavin and selenium on central nervous system oxygen toxicity.

作者信息

Boadi W Y, Thaire L, Kerem D, Yannai S

机构信息

Department of Food Engineering and Biotechnology, Technion-Israel Institute of Technology, Haifa.

出版信息

Pharmacol Toxicol. 1991 Feb;68(2):77-82. doi: 10.1111/j.1600-0773.1991.tb02039.x.

DOI:10.1111/j.1600-0773.1991.tb02039.x
PMID:1852722
Abstract

We attempted to modify the resistance of rats to hyperbaric oxygen (HBO)-induced central nervous system (CNS) toxicity, by increasing the tissue antioxidant potential through dietary factors. Groups of rats were fed excesses of vitamin E (VIT E) alone or in combinations with riboflavin (RIB), selenium (Se) or both, for 30 days. A control group was maintained on an unsupplemented diet. On the 23rd day animals to be exposed were implanted with chronic electrodes for electrocorticographic (ECoG) recording. Later, each group was divided into two subgroups, of which one was exposed to 4.5 atmospheres absolute (ATA) of 100% oxygen (O2) for 30 min., hereafter referred to as "exposed", noting the time of appearance of first electrical discharge (FED) in their ECoG. The remaining subgroups were left unexposed. Forty-eight hours later, all animals were sacrificed and some of their tissues were analyzed for glutathione (GSH). The GSH level in the liver, brain, lungs and blood of all experimental subgroups were significantly higher than in the control unexposed counterparts. Combinations of RIB and/or Se with VIT E failed to show a greater increase in GSH over VIT E alone. This increase was, however, not accompanied by a meaningful delay in the appearance of FED. Forty-eight hours post-exposure, the brain GSH levels of all exposed subgroups were still lower than the respective pre-exposure levels. Yet, in the treated exposed subgroups the GSH levels observed 48 hr after exposure were already higher than in the untreated unexposed controls.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们试图通过饮食因素提高组织抗氧化能力,来改变大鼠对高压氧(HBO)诱导的中枢神经系统(CNS)毒性的抵抗力。将大鼠分组,单独给予过量维生素E(VIT E)或与核黄素(RIB)、硒(Se)联合给予,持续30天。对照组维持不补充饮食。在第23天,将接受暴露的动物植入慢性电极用于脑电描记(ECoG)记录。之后,每组分为两个亚组,其中一个亚组暴露于4.5绝对大气压(ATA)的100%氧气(O2)中30分钟,以下简称“暴露组”,记录其ECoG中首次放电(FED)出现的时间。其余亚组不进行暴露。48小时后,处死所有动物,分析部分组织中的谷胱甘肽(GSH)。所有实验亚组肝脏、脑、肺和血液中的GSH水平均显著高于未暴露的对照亚组。RIB和/或Se与VIT E联合使用时,GSH的增加幅度并未超过单独使用VIT E。然而,这种增加并未伴随FED出现时间的显著延迟。暴露后48小时,所有暴露亚组的脑GSH水平仍低于各自暴露前的水平。然而,在接受治疗的暴露亚组中,暴露后48小时观察到的GSH水平已经高于未接受治疗的未暴露对照组。(摘要截短于250字)

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