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[碘和铜缺乏条件下甲状腺功能减退大鼠脂质和蛋白质自由基氧化过程及抗氧化防御的变化]

[The changes of processes of free radical oxidation of lipids and proteins, antioxidant defence in rats with hypofunction of the thyroid gland in conditions of iodine and copper deficiency].

作者信息

Voronych-Semchenko N M, Huranych T V

出版信息

Fiziol Zh (1994). 2014;60(4):30-9.

Abstract

Thyroid status, copper balance, correlation of processes of peroxide oxidation of lipids (POL), proteins (POP), antioxidant defence (AOD) were examined in experiments on rats with hypofunction of thyroid gland under iodine monodeficit (HTGI) and combined iodine and copper deficit (HTGI+Cu). It was determined that a combined deficit of microelements is accompanied by a distribution of copper content between different tissues (increase in red blood cell mass and cerebrum, decrease in myocardium), essential changes of indexes of hypotalamo-hypophysis-thyroid axis, oxygen-dependent metabolism, antiradical defense, exacerbating the effects of negative influence of each of them on organism. It was established that HTGI+Cu causes a suppression of oxygen-dependent processes. In thyroid gland, it is shown a decrease of content of dyenic conjugates (DC) by 69,70% , of TBA-reacting products (TBA-RP) by 47,72% in diencephalon, the volume of modified proteins (VMP) - by 37,10-98,98% in the tissues of diencephalons. The results obtained let us to suggest a pivotal role ofmicroelement dysbalance and metabolic mechanisms in pathogenesis of cardiological pathology under thyroid dysfunction. The development of HTGI +Cu exhausts the resources of AOD: decreases the activity of catalase (on 47,05%), superoxide dismutase (on 33,13%), ceruloplasmine (on 33,93%) and saturation of transferrin with iron (on 56,76%) against the background of selective rise in the activity of glu-tationreductase (in 2,8 time) in comparison with the control data. The long-term disturbances ofantyoxidative defence can be the reason of manifestation of oxygendependent processes and the development of pathological changes in separate physiological systems of organism.

摘要

在碘缺乏(HTGI)以及碘和铜联合缺乏(HTGI+Cu)导致甲状腺功能减退的大鼠实验中,对甲状腺状态、铜平衡、脂质过氧化过程(POL)、蛋白质过氧化过程(POP)以及抗氧化防御(AOD)进行了检测。结果表明,微量元素联合缺乏伴随着铜在不同组织间的重新分布(红细胞和大脑中铜含量增加,心肌中铜含量减少),下丘脑-垂体-甲状腺轴指标、氧依赖代谢、抗自由基防御发生显著变化,加剧了它们各自对机体负面影响的效应。已证实,HTGI+Cu会抑制氧依赖过程。在甲状腺中,二烯共轭物(DC)含量降低了69.70%,在间脑中,TBA反应产物(TBA-RP)含量降低了47.72%,间脑组织中修饰蛋白体积(VMP)降低了37.10% - 98.98%。所得结果提示,微量元素失衡和代谢机制在甲状腺功能障碍导致的心脏病理发病机制中起关键作用。HTGI +Cu的发展耗尽了AOD的资源:与对照数据相比,在谷胱甘肽还原酶活性选择性升高(2.8倍)的背景下,过氧化氢酶活性降低了47.05%,超氧化物歧化酶活性降低了33.13%,铜蓝蛋白活性降低了33.93%,转铁蛋白铁饱和度降低了56.76%。抗氧化防御的长期紊乱可能是氧依赖过程表现以及机体各生理系统发生病理变化的原因。

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