本文選題：硒 + 碘　； 參考：《汕頭大學(xué)》2005年碩士論文

【摘要】：背景與目的 硒是人和動(dòng)物生命活動(dòng)所必需的微量元素。硒缺乏會(huì)引起含硒酶活性降低, 氧自由基清除受阻、內(nèi)分泌紊亂等一系列機(jī)體功能障礙,其對(duì)神經(jīng)系統(tǒng)的影響也 越來(lái)越引起學(xué)者們的重視。硒缺乏與碘缺乏密切相關(guān),低碘地區(qū)常同時(shí)伴有低 硒。在政府二十多年的全民補(bǔ)碘后,碘缺乏所致的典型的克汀病已基本得到控制, 但是仍有許多亞臨床克汀病弱智兒童出現(xiàn),故認(rèn)為硒可能是亞克汀病的一個(gè)重要 的碘外因素。 既往硒、碘缺乏的動(dòng)物實(shí)驗(yàn)研究多集中于原代及仔一代,且多為成年期。為 模擬硒碘缺乏病區(qū)人口世代生存繁衍于低硒或聯(lián)合低碘環(huán)境所致的長(zhǎng)期損害,尤 其是對(duì)子代兒童所致的智力損害,我們與多方學(xué)者共同合作建立了人工膳食低硒 低碘喂養(yǎng)繁殖的SD大鼠動(dòng)物模型,并歷時(shí)近兩年繁衍至仔四代。本模型仔三代 大鼠已經(jīng)表現(xiàn)出不同程度神經(jīng)行為發(fā)育延遲、Morris水迷宮的空間學(xué)習(xí)記憶能 力降低,并表明低硒對(duì)大鼠腦EGFR/MAPK信號(hào)傳導(dǎo)通路有一定影響,等等。為進(jìn) 一步研究長(zhǎng)期低硒低碘對(duì)仔代發(fā)育期大鼠的生長(zhǎng)發(fā)育和神經(jīng)行為發(fā)育影響的生 化分子機(jī)制,我們對(duì)仔三、四代發(fā)育期大鼠肝臟、全血、多腦區(qū)抗氧化酶系統(tǒng)及 腦中單胺類神經(jīng)遞質(zhì)進(jìn)行了測(cè)定。 方法 選取本課題組已成功建立的人工膳食低硒低碘喂養(yǎng)繁殖的SD大鼠動(dòng)物模 型,仔三(F3)、四代(F4)新生4天(P4)和21天(P21)大鼠。模型分4組:(1)對(duì) 照組(Control組),硒水平0.1-0.3μ g/g,碘水平≥0.2μ g/g;(2)低硒組(Se- 組),硒水平0.02 μ g/g,碘水平≥0.2 μ g/g;(3)低碘組(I-組),硒水平0.1-
[Abstract]:Background and purpose Selenium is an essential trace element for human and animal life. Selenium deficiency causes a decrease in the activity of selenase, Oxygen free radical clearance blocked, endocrine disorders and a series of functional disorders, its impact on the nervous system is also More and more scholars pay attention to it. Selenium deficiency is closely related to iodine deficiency, which is often accompanied by low iodine deficiency. Selenium. After more than 20 years of universal iodine supplementation by the government, the typical cretinism caused by iodine deficiency has been basically brought under control. However, there are still many children with subclinical cretinism and mental retardation, so it is believed that selenium may be an important factor in subcretinism. The extraiodine factor. Previous studies on selenium and iodine deficiency focused on the primary generation and the offspring, and most of them were adult. For Long-term damage caused by simulated selenium and iodine deficiency disorders in populations living for generations in low selenium or combined iodine deficiency environments, especially It is a kind of intellectual damage to the children of offspring. We have worked with many scholars to establish the artificial diet with low selenium. The SD rat model was fed with iodine deficiency and lasted for nearly two years until the fourth generation. The third generation of this model Spatial learning and memory ability of Morris water maze with different degrees of neurobehavioral retardation in rats The effect of selenium deficiency on the EGFR/MAPK signal transduction pathway in the rat brain was decreased, and so on. To advance One-step study on the effects of long-term selenium and iodine deficiency on the growth and neurobehavioral development of rats in their offspring development The molecular mechanism of antioxidation enzymes in the liver, whole blood, multibrain regions of rats in the third and fourth generation of pups The monoamine neurotransmitters in the brain were determined. Method Selected SD rat model of artificial diet fed with low selenium and iodine, which has been successfully established by our research group P4) and P21 (21 days after birth) of the third generation of F _ 3 (F _ 4) and 21 days (P _ (4) (P _ (4) (P _ (4) and P _ (1). The model is divided into 4 groups: 1) Selenium level 0.1-0.3 渭 g / g, iodine level 鈮，

本文編號(hào)：1949113