本文選題：過氯酸銨　切入點：甲狀腺　出處：《華中科技大學》2012年碩士論文　論文類型：學位論文

【摘要】：目的過氯酸銨（Ammonium Perchlorate，AP）是一種白色晶體粉末，是導彈和火箭復合固體推進劑的重要組分，被廣泛應用于航天航空工業(yè)和國防工業(yè)。AP在生產(chǎn)和使用中會散出大量的粉塵，通過不同的途徑進入機體產(chǎn)生健康損害。已有研究發(fā)現(xiàn)AP可致甲狀腺結(jié)構發(fā)生改變，并影響其正常功能。本實驗室曾有研究發(fā)現(xiàn)AP可影響大鼠甲狀腺激素的分泌以及鈉碘轉(zhuǎn)運體的表達。本實驗旨在探討過氯酸銨對大鼠體內(nèi)碘負荷和抗氧化能力的影響，闡述其毒作用機制，為預防和控制過氯酸銨對職業(yè)人群的健康危害、保護工人健康提供科學依據(jù)。 方法將SD雄性大鼠20只隨機分成4組，即對照組、AP低劑量組、中劑量組和高劑量組，每組5只。染毒劑量分別為0、130、260、520mg·kg~(-1)·d~(-1)，，經(jīng)口飲水染毒。每周定時稱量體重1次，并依據(jù)體重計算AP染毒量，持續(xù)染毒13周。于染毒第6周和第13周時，分別采用擠壓膀胱反射排尿法采集大鼠尿液，用尿碘砷鈰催化分光光度法檢測大鼠尿碘水平。染毒13周后處死并解剖大鼠，取甲狀腺、心、肝、脾、肺、腎及睪丸，分別稱重，并計算臟器系數(shù)。取部分甲狀腺組織，采用食物中碘的測定法檢測甲狀腺組織總碘量、相對含碘量。取部分甲狀腺組織勻漿,試劑盒檢測蛋白定量、丙二醛（MDA）、超氧化物歧化酶（SOD）、甲狀腺過氧化氫酶（CAT）等指標。 結(jié)果大鼠經(jīng)AP染毒至13周，高、中劑量組大鼠的體重增長明顯低于對照組，差異有統(tǒng)計學意義（P0.05）；各劑量組的甲狀腺臟器系數(shù)均顯著高于對照組，差異有統(tǒng)計學意義（P0.01）；染毒第6周AP高劑量組尿碘水平比對照組明顯升高（P0.05），而染毒第13周各劑量組尿碘水平與對照組比較均無明顯差別（P0.05）。染毒至第13周，各劑量組甲狀腺總碘量均明顯低于對照組，差異有統(tǒng)計學意義（P0.01）；各劑量組相對含碘量明顯低于對照組，并隨染毒劑量的升高而逐漸下降，差異有統(tǒng)計學意義（P0.01）；AP染毒各劑量組甲狀腺總蛋白定量水平與對照組相比均有下降，但僅中、高劑量組差異具有統(tǒng)計學意義（P0.05）；各劑量組MDA含量與對照組比較均無明顯差異（P0.05）；而各劑量組SOD活力與對照組相比均有升高，但其差異尚不顯著（P0.05）；AP低、中、高劑量組大鼠CAT活力與對照組相比，呈逐漸升高趨勢，但只有高劑量組與對照組相比具有統(tǒng)計學意義（P0.01）。 結(jié)論本研究通過AP染毒大鼠13周表明，AP對大鼠具有毒作用，其靶器官為甲狀腺。AP可競爭性抑制甲狀腺攝取碘，使甲狀腺攝碘不足，在一定時間內(nèi)表現(xiàn)為大鼠尿碘增加，并致甲狀腺組織含碘量降低，進而導致甲狀腺組織代償性增生腫大和體重增長遲緩。另外，AP可致甲狀腺蛋白定量水平減少，并對甲狀腺組織造成氧化損傷，引起甲狀腺過氧化氫酶活性升高。以上結(jié)果均表明，AP對甲狀腺具有明顯的毒作用，為進一步闡明AP對健康的危害提供了可靠的實驗依據(jù)。
[Abstract]:Objective Ammonium Perchlorate APs is a kind of white crystal powder, which is an important component of missile and rocket composite solid propellant. It is widely used in aerospace industry and national defense industry. Health damage is caused by entering the body in different ways. It has been found that AP can cause changes in thyroid structure. It has been found that AP can affect the secretion of thyroid hormone and the expression of sodium iodide transporter in rats. The aim of this study was to investigate the effects of ammonium perchlorate on iodine load and antioxidant capacity in rats. The mechanism of toxic effect of ammonium perchlorate is described in order to provide scientific basis for preventing and controlling the health hazard of ammonium perchlorate to occupational population and protecting the health of workers. Methods Twenty Sprague-Dawley male rats were randomly divided into 4 groups: control group with low dose of AP, medium dose group and high dose group with 5 rats in each group. The dosage of AP was calculated according to body weight for 13 weeks. At the 6th and 13th weeks of exposure, the urine of rats was collected by pressing bladder reflex urination method. Urinary iodine level was determined by catalytic spectrophotometry. After 13 weeks of exposure, rats were killed and dissected. Thyroid gland, heart, liver, spleen, lung, kidney and testis were weighed, and organ coefficients were calculated. The total iodine content and relative iodine content of thyroid tissue were determined by the method of determination of iodine in food. Some thyroid tissue homogenate was taken, the protein quantity was detected by kit, malondialdehyde (MDA) MDAA, superoxide dismutase (SOD) and catalase (CAT) were measured. Results the weight gain of rats in the middle dose group was significantly lower than that in the control group (P 0.05), and the thyroid organ coefficient of each dose group was significantly higher than that of the control group, the rats were exposed to AP for 13 weeks, and the weight gain in the middle dose group was significantly lower than that in the control group (P 0.05). The level of urinary iodine in the AP high dose group was significantly higher than that in the control group at the 6th week of exposure, but there was no significant difference in urinary iodine level between the control group and the control group at the 13th week after exposure, and the level of urinary iodine in the AP high dose group was not significantly different from that in the control group from the 13th week to the 13th week. The total iodine content of thyroid in each dose group was significantly lower than that in the control group, the difference was statistically significant (P 0.01), the relative iodine content in each dose group was significantly lower than that in the control group, and gradually decreased with the increase of the dose. The difference was statistically significant (P 0.01). The quantitative level of thyroid total protein in each dose group was lower than that in the control group, but it was only moderate. There was no significant difference in the content of MDA between the high dose group and the control group (P 0.05), but the activity of SOD in each dose group was higher than that in the control group, but the difference was not significant (P 0.05), but the difference was not significant (P 0.05). Compared with the control group, the activity of CAT in the high dose group was gradually increased, but only in the high dose group compared with the control group, there was a statistically significant difference between the high dose group and the control group (P 0.01). Conclusion in this study, the rats exposed to AP for 13 weeks showed that AP had toxic effect on rats. The target organ of AP was thyroid. AP could competitively inhibit thyroid uptake of iodine, which resulted in insufficient uptake of iodine by thyroid, and increased urinary iodine in rats in a certain period of time. The iodine content of thyroid tissue was decreased, which resulted in compensatory hyperplasia of thyroid tissue and slow weight gain. AP also decreased the quantitative level of thyroid protein and caused oxidative damage to thyroid tissue. The above results indicate that AP has obvious toxic effect on thyroid gland, which provides a reliable experimental basis for further elucidating the harm of AP to health.
【學位授予單位】：華中科技大學
【學位級別】：碩士
【學位授予年份】：2012
【分類號】：R114

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