發(fā)布時(shí)間：2018-07-01 12:50

  本文選題：醋酸鉛 + 亞硒酸鈉　； 參考：《東北農(nóng)業(yè)大學(xué)》2017年碩士論文

【摘要】：鉛是有毒的重金屬之一,在工業(yè)中被廣泛應(yīng)用。鉛能引起環(huán)境污染,并且能在人類(lèi)和動(dòng)物體內(nèi)蓄積,影響人類(lèi)和動(dòng)物健康。硒是人類(lèi)和動(dòng)物體內(nèi)一種必需的營(yíng)養(yǎng)微量元素,能緩解鉛引起的毒性。本實(shí)驗(yàn)旨在研究硒對(duì)雞睪丸鉛中毒的緩解作用,為以后研究硒緩解鳥(niǎo)類(lèi)睪丸鉛中毒提供了參考。本試驗(yàn)將180只1日齡海蘭蛋公雞預(yù)飼1周后隨機(jī)分成4組。對(duì)照組飼喂標(biāo)準(zhǔn)商品日糧(含硒為0.49mg/kg)和飲用水;硒組飼喂添加亞硒酸鈉(含硒為1 mg/kg)的標(biāo)準(zhǔn)商品日糧和飲用水;鉛組飼喂標(biāo)準(zhǔn)商品日糧和添加醋酸鉛(含鉛為350 mg/L)的飲用水;鉛硒組飼喂添加亞硒酸鈉的標(biāo)準(zhǔn)商品日糧(含硒為0.49 mg/kg)和添加醋酸鉛的飲用水(含鉛為350mg/L)。在試驗(yàn)的第30天、60天和90天,在每組中隨機(jī)選取15只雞處死并摘取睪丸組織。檢測(cè)了30天、60天和90天的谷胱甘肽過(guò)氧化物酶(GPx)、超氧化物歧化酶(SOD)、過(guò)氧化氫酶(CAT)、總抗氧化能力(T-AOC)、谷胱甘肽轉(zhuǎn)移酶(GST)活力,谷胱甘肽(GSH)、丙二醛(MDA)和過(guò)氧化氫(H_2O_2)含量;一氧化氮(NO)含量和一氧化氮合酶(i NOS)活力;核轉(zhuǎn)錄因子(NF-κB)、環(huán)氧合酶-2(COX-2)、腫瘤壞死因子(TNF-α)、前列腺素E合成酶(PTGEs)、i NOS、白介素(IL)-2、IL-4、IL-6、IL-12β、IL-17和干擾素(IFN)-γ的m RNA水平、組織學(xué)和超微結(jié)構(gòu)的變化;90天的鉛和硒的濃度、NF-κB、i NOS、熱休克蛋白(HSP)60、HSP70、HSP90蛋白水平和超微結(jié)構(gòu)變化。得出如下結(jié)論:(1)鉛中毒增加了睪丸組織鉛濃度,降低了硒濃度,引起了睪丸鉛積累;引起了雞睪丸曲精細(xì)管和生殖細(xì)胞變形,部分生殖細(xì)胞散落到管腔,并且有炎性細(xì)胞浸潤(rùn)的出現(xiàn)。超微結(jié)構(gòu)上發(fā)現(xiàn),精母細(xì)胞核仁消失,間質(zhì)細(xì)胞形狀不規(guī)則,染色質(zhì)邊緣化以及線粒體空泡,引起了睪丸組織損傷;硒緩解了鉛中毒誘導(dǎo)的上述變化,硒緩解了過(guò)量鉛引起的雞睪丸鉛積累及睪丸損傷。(2)鉛中毒上調(diào)了HSP60、HSP70和HSP90的蛋白質(zhì)表達(dá),硒緩解了鉛中毒上調(diào)的雞睪丸HSPs的蛋白質(zhì)表達(dá),結(jié)果說(shuō)明鉛中毒時(shí),機(jī)體動(dòng)員了熱休克蛋白來(lái)抵御了鉛的毒性,硒緩解了鉛中毒。(3)鉛中毒誘導(dǎo)了雞睪丸NF-κB、COX-2、TNF-α、PTGEs、i NOS、IL-4、IL-6、IL-12β和IL-17 m RNA表達(dá),NO含量和i NOS活力,誘導(dǎo)了NF-κB和i NOS蛋白表達(dá),引起了炎癥反應(yīng);降低了IL-2和IFN-γm RNA表達(dá),引起了免疫抑制;硒緩解了鉛中毒誘導(dǎo)的炎癥相關(guān)因子表達(dá)的變化,緩解了雞睪丸炎癥反應(yīng)和免疫抑制。(4)鉛中毒降低了雞睪丸SOD、GPx、CAT、T-AOC和GST活力,GSH含量,增加了MDA和H_2O_2含量,引起了氧化應(yīng)激;硒緩解了鉛中毒引起的氧化應(yīng)激指標(biāo)的變化,緩解了雞睪丸氧化應(yīng)激。
[Abstract]:Lead is one of the toxic heavy metals and is widely used in industry. Lead causes environmental pollution and accumulates in humans and animals, affecting human and animal health. Selenium is an essential nutrient trace element in human and animal, which can alleviate the toxicity caused by lead. The aim of this study was to study the effect of selenium on the remission of lead poisoning in the testis of chickens, and to provide a reference for the later study on the alleviation of lead poisoning in the testis of birds. 180 1-day-old Hailan egg cocks were randomly divided into 4 groups after 1 week of prefeeding. The control group was fed with standard commercial diet (selenium containing 0.49mg/kg) and drinking water, the selenium group was fed with standard commercial diet and drinking water supplemented with sodium selenite (containing 1 mg/kg of selenium), the lead group was fed with standard commercial diet and drinking water with lead acetate (350mg / L). The lead selenium group was fed with standard diet containing sodium selenite (0.49 mg/kg) and drinking water with lead acetate (350 mg / L lead). On the 30th day, 60 days and 90 days, 15 chickens were randomly selected to be killed and testicular tissues were removed. The contents of glutathione peroxidase (GPX), superoxide dismutase (SOD), catalase (cat), total antioxidant capacity (T-AOC), glutathione transferase (GST), glutathione (GSH), malondialdehyde (MDA) and hydrogen peroxide (H _ 2O _ 2) were measured at 30 and 90 days. Content of nitric oxide (no) and activity of nitric oxide synthase (iNOS), mRNA levels of nuclear transcription factor (NF- 魏 B), cyclooxygenase-2 (COX-2), tumor necrosis factor (TNF- 偽), prostaglandin E synthase (PTGEs), IL-6IL-12 尾 IL-17 and interferon (IFN)-緯, Histopathological and ultrastructural changes of lead and selenium concentrations NF- 魏 Bnos, heat shock protein (HSP60) HSP70HSP90 protein levels and ultrastructural changes were observed at 90 days. The conclusions are as follows: (1) lead poisoning increased lead concentration in testis, decreased selenium concentration, caused lead accumulation in testis, caused deformation of testicular tubules and germ cells, and scattered some germ cells into the lumen. And inflammatory cell infiltration appeared. Ultrastructural findings showed that spermatocyte nucleolus disappeared, interstitial cells were irregular in shape, chromatin was marginalized and mitochondria vacuole, which caused testicular tissue damage, selenium alleviated the above changes induced by lead poisoning. Selenium alleviated the lead accumulation and testicular damage induced by excessive lead. (2) lead poisoning upregulated the protein expression of HSP60, HSP70 and HSP90, and selenium alleviated the up-regulated protein expression of HSPs in the testis of lead poisoning. Heat shock protein was mobilized to resist lead toxicity and selenium alleviated lead poisoning. (3) lead poisoning induced the expression of nitric oxide (no), IL-6, IL-12 尾 and IL-17 mRNA, and induced the expression of NF- 魏 B and iNOS protein, and induced inflammatory reaction. Selenium alleviated the expression of inflammatory related factors induced by lead poisoning, and alleviated the inflammatory reaction and immunosuppression of chicken testis. (4) lead poisoning decreased the contents of T-AOC and GSH of T-AOC and GST activity in testis. The contents of MDA and H _ 2O _ 2 were increased and oxidative stress was induced by selenium. Selenium alleviated the changes of oxidative stress index caused by lead poisoning and alleviated oxidative stress in testis of chicken.
【學(xué)位授予單位】：東北農(nóng)業(yè)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：S858.31

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