發(fā)布時(shí)間：2023-04-16 23:01

　　近年來(lái),隨著工農(nóng)業(yè)的快速發(fā)展,大量危害動(dòng)物生存環(huán)境和人類(lèi)健康的化學(xué)品被釋放到自然環(huán)境中。大量證據(jù)表明,空氣、土壤和水域中許多化學(xué)污染物正在干擾野生動(dòng)物和人類(lèi)的正常生理活動(dòng)。據(jù)報(bào)道,兩棲動(dòng)物種群數(shù)量在全球范圍內(nèi)正在急劇下降,其中人工合成化學(xué)物質(zhì)對(duì)環(huán)境的污染是主要因素之一。兩棲動(dòng)物的繁殖和幼體發(fā)育在水環(huán)境中完成,水域化學(xué)污染物可能以致死劑量直接導(dǎo)致動(dòng)物死亡,也可能通過(guò)亞致死劑量影響動(dòng)物的代謝、免疫以及繁殖等機(jī)能。有機(jī)磷類(lèi)殺蟲(chóng)劑(organophosphate insecticides,OPs)是繼有機(jī)氯類(lèi)被禁用后應(yīng)用最為廣泛的一類(lèi)農(nóng)藥。它具有廣譜、高效、殘留期短以及使用成本低等特點(diǎn),已成為當(dāng)前主要的農(nóng)藥種類(lèi),占全球殺蟲(chóng)劑使用總量的70%以上。敵百蟲(chóng)(trichlorphon),化學(xué)名O,O-二甲基-(2,2,2-三氯-1-羥基乙基)磷酸酯(C4H8O4C13P),是一種最常見(jiàn)的有機(jī)磷農(nóng)藥,被廣泛用于害蟲(chóng)防治以及養(yǎng)殖動(dòng)物體內(nèi)外寄生蟲(chóng)的殺滅。在水產(chǎn)養(yǎng)殖中,敵百蟲(chóng)通常用于防治水生昆蟲(chóng)對(duì)養(yǎng)殖對(duì)象的感染以及體外的蠕蟲(chóng)寄生,也可用于控制水體中的浮游生物的過(guò)度繁殖。然而,長(zhǎng)期反復(fù)的使用將形成敵百蟲(chóng)對(duì)水源...

【文章頁(yè)數(shù)】：111 頁(yè)

【學(xué)位級(jí)別】：博士

【文章目錄】：
摘要
Abstract
Chapter Ⅰ Rview on toxic mechanisms of organophosphate insecticidestowards non-target aquatilia
    1.1 Summary of OPs
        1.1.1 Physical and chemical properties of OPs
        1.1.2 The mechanism of OPs towards non-target organisms
    1.2 The toxic mechanisms of OPs towards non-target aquatilia
        1.2.1 The toxic effects of OPs towards non-target aquatilia
        1.2.2 Neurotoxicity and behaviors effect of OPs
        1.2.3 Endocrine, reproductive and developmental disruption effects of OPs
        1.2.4 Oxidative stress and histopathological responses of OPs
        1.2.5 Genotoxic effects and DNA damage of OPs
        1.2.6 Immunological responses of OPs
    1.3 Toxic mechanisms of OPs towards non-target aquatilia
    1.4 Studies of amphibians in ecotoxicology
    1.5 The purpose and significance of this study
Chapter Ⅱ Evaluation of toxic and genotoxic effects of low doses oftrichlorfon on Rana chensinensis tadpoles
    2.1 Introduction
    2.2 Materials and methods
        2.2.1 Experimental animals and treatments
        2.2.2 Tests of survival, growth, development and abnormalities
        2.2.3 Tests for micronucleus formation and nuclear abnormalities
        2.2.4 Single-cell gel electrophoresis assay
        2.2.5 DNA ladder assay
        2.2.6 Statistical analysis
    2.3 Results
        2.3.1 Analysis of survival, growth, development and morphological abnormalities
        2.3.2 Micronuclei assay
        2.3.3 DNA damage induced by trichlorfon
        2.3.4 DNA fragmentation induced by trichlorfon
    2.4 Discussion
    2.5 Conclusion
Chapter Ⅲ Oxidative stress and hepatotoxicity in the frog, Ranachensinensis, when exposed to low doses of trichlorfon
    3.1 Introduction
    3.2 Materials and methods
        3.2.1 Chemicals and reagents
        3.2.2 Animals and treatments
        3.2.3 Biological assays
        3.2.4 Pathological analysis
        3.2.5 Statistical analysis
    3.3 Results
        3.3.1 Analysis of antioxidant enzyme activity
        3.3.2 Histocytopathological analysis
    3.4 Discussion
    3.5 Conclusion
Chapter Ⅳ Transcriptome analysis of Rana chensinensis liver undertrichlorfon stress
    4.1 Introduction
    4.2 Materials and methods
        4.2.1 Animals and treatments
        4.2.2 RNA isolation and deep sequencing
        4.2.3 Bioinformatics analysis
    4.3 Results
        4.3.1 Sequencing and de novo assembly
        4.3.2 Functional annotation of unigenes
        4.3.3 KEGG pathway analysis
    4.4 Discussion
    4.5 Conclusion
Chapter Ⅴ Identification and validation of DEGs induced by trichlorfonstress in Rana chensinensis Liver
    5.1 Introduction
    5.2 Materials and methods
        5.2.1 Animals and treatments
        5.2.2 Identification of differentially expressed genes (DEGs)
        5.2.3 Validation of RNA-seq profiles by qPCR
    5.3 Results
        5.3.1 Identification of DEGs induced by trichlorfon stress
        5.3.2 Validation of RNA-seq profiles by qPCR
    5.4 Discussion
    5.5 Conclusion
Chapter Ⅵ Summary and conclusions
References
Supporting information
Acknowledgements
Publications



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