發(fā)布時間：2018-06-13 20:36

  本文選題：鎘 + 雞胚　； 參考：《東北農(nóng)業(yè)大學(xué)》2017年碩士論文

【摘要】：鎘是環(huán)境中毒性最強的污染物之一,其隨著食物鏈的傳遞在動物或人體內(nèi)富集,最終引起多種器官和組織的損傷。研究表明鎘能透過胎盤屏障進入胚胎并危害早期神經(jīng)系統(tǒng)發(fā)育,但其毒性機制仍不清楚。本研究以HH-4期雞胚為試驗?zāi)Ｐ?通過卵黃注射方式進行鎘暴露,觀察HH-12期雞胚整體及神經(jīng)管發(fā)育情況,檢測雞胚組織抗氧化功能與Nrf2抗氧化防御應(yīng)答相關(guān)因子,結(jié)果顯示:鎘暴露能夠引起早期雞胚死亡率增加、HH-0至HH-12期發(fā)育時間延長、胚胎畸形率顯著增加,表明鎘導(dǎo)致雞胚發(fā)育遲滯與畸形,具有顯著的胚胎發(fā)育毒性。鎘暴露能夠引起早期雞胚神經(jīng)管標志因子Shh表達量升高,而Pax3和Pax7表達量降低,隨著鎘濃度增加雞胚神經(jīng)管呈現(xiàn)不程度的閉合不全,表明鎘誘發(fā)神經(jīng)管發(fā)育異常,這可能是鎘早期胚胎神經(jīng)發(fā)育毒性的重要機制之一。鎘暴露引起雞胚組織中MDA和H_2O_2含量增加,SOD、CAT、GSH-Px活性與GSH含量顯著降低,T-AOC水平下降,表明鎘能夠增加自由基與脂質(zhì)過氧化物含量,降低抗氧化酶活性,擾亂雞胚抗氧化防御系統(tǒng),最終引發(fā)氧化應(yīng)激,這可能是其致早期胚胎神經(jīng)管閉合不全的重要機制之一。低劑量鎘暴露能夠增強Nrf2表達水平,并介導(dǎo)Ⅱ相解毒酶NQO1、HO-1、CAT、GST、GCLC、GCLM、SOD1-3轉(zhuǎn)錄增加,而高劑量鎘暴露能夠抑制這一效應(yīng),表明鎘能夠通過激發(fā)Nrf2介導(dǎo)的抗氧化防御應(yīng)答來拮抗氧化應(yīng)激,揭示Nrf2抗氧化防御應(yīng)答在鎘致雞胚早期神經(jīng)發(fā)育中的具有保護作用。
[Abstract]:Cadmium is one of the most toxic pollutants in the environment. With the transfer of food chain, cadmium is enriched in animal or human body, and eventually causes damage to many organs and tissues. It has been shown that cadmium can enter the embryo through placental barrier and endanger the early development of nervous system, but the mechanism of cadmium toxicity is still unclear. In this study, HH-4 stage chicken embryo was used as experimental model. Cadmium exposure was carried out by yolk injection. The development of whole embryo and nerve tube of HH-12 stage chicken embryo was observed. The antioxidant function of chicken embryo and the related factor of Nrf2 antioxidation defense response were detected. The results showed that cadmium exposure could increase the death rate of early chicken embryos and prolong the development time from HH-0 to HH-12, and the rate of embryo malformation was significantly increased, which indicated that cadmium could cause delayed and abnormal development of chicken embryos and had significant developmental toxicity. Cadmium exposure could increase the expression of neural tube marker factor Shh, but decrease the expression of Pax3 and Pax7 in early chicken embryo. With the increase of cadmium concentration, the neural tube of chicken embryo showed incomplete closure, which indicated that cadmium induced abnormal development of neural tube. This may be one of the important mechanisms of neurotoxicity in cadmium early embryo. The contents of MDA and H2O2 in chicken embryo tissue were increased by cadmium exposure. The activity of GSH-Px and the content of GSH decreased significantly, which indicated that cadmium could increase the content of free radical and lipid peroxide, decrease the activity of antioxidant enzyme, and disrupt the antioxidant defense system of chicken embryo. Oxidative stress may be one of the important mechanisms of neural tube insufficiency in early embryo. Low dose cadmium exposure enhanced the expression of Nrf2 and mediated the increase of transcription of phase 鈪，

本文編號：2015332