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外源α-生育酚提高青綠苔草耐鹽性生理機制的研究

發(fā)布時間:2018-08-27 12:41
【摘要】:土壤鹽堿化會嚴(yán)重影響植物的生長發(fā)育,通過外源化學(xué)物質(zhì)調(diào)控減少鹽脅迫對植物的傷害,提高植物自身對鹽堿環(huán)境的適應(yīng)能力,對于促進鹽脅迫下植物的正常生長發(fā)育以及鹽堿地綠化具有重要意義。α-生育酚是綠色植物重要的脂溶性抗氧化劑之一,是植物在逆境下細(xì)胞膜上重要的效應(yīng)物。本研究以青綠苔草(Carex leucochlora)為試驗材料,研究不同濃度外源α-生育酚對鹽(0.8%NaCl)脅迫下青綠苔草植株生長抑制及傷害的緩解作用;并在此基礎(chǔ)上,研究了外源α-生育酚對鹽脅迫下青綠苔草體內(nèi)活性氧代謝、滲透調(diào)節(jié)以及光合代謝的影響。旨在揭示外源α-生育酚在提高青綠苔草耐鹽性中發(fā)揮的主要生理調(diào)節(jié)功能,并為生產(chǎn)上增強植物的抗鹽性提供一定的理論依據(jù)。本研究結(jié)果如下:1.適宜濃度的外源α-生育酚處理可以緩解鹽脅迫對青綠苔草生長和質(zhì)膜的傷害,并進一步提高其內(nèi)源生育酚的含量。鹽脅迫下青綠苔草的生長和質(zhì)膜均受到傷害,且內(nèi)源生育酚含量顯著提高;0.2mM~1.0mMα-生育酚均能不同程度地增加鹽脅迫下青綠苔草的株高和干物質(zhì)的積累,降低丙二醛(MDA)含量和質(zhì)膜相對透性,并且進一步提高其內(nèi)源生育酚含量。其中以0.8mM的外源α-生育酚對鹽脅迫傷害的緩解作用效果最佳,且在此濃度下青綠苔草內(nèi)源生育酚含量最高。2.外源α-生育酚可以通過提高青綠苔草抗氧化酶活性以及改善抗壞血酸-谷胱甘肽循環(huán)來降低鹽脅迫下植株體內(nèi)過多活性氧的積累。鹽脅迫下青綠苔草體內(nèi)活性氧水平顯著增加,抗氧化酶超氧化物歧化酶(SOD)、過氧化氧酶(CAT)活性以及非酶促抗氧化物質(zhì)抗壞血酸(ASA)和谷胱甘肽(GSH)含量變化均呈先上升后下降的趨勢,而ASA/DHA和GSH/GSSG比值均顯著下降;外源噴施α-生育酚提高了鹽脅迫下青綠苔草抗氧化酶SOD、過氧化物酶(POD)和CAT的活性,ASA和GSH含量增加,ASA/DHA和GSH/GSSG比值增大,同時植株體內(nèi)抗壞血酸氧化酶(APX)、谷胱甘肽還原酶(GR)和脫氧抗壞血酸還原酶(DHAR)活性顯著升高。這些結(jié)果說明,鹽脅迫下α-生育酚不僅可以通過提高抗氧化酶活性來降低植株體內(nèi)過多的活性氧,同時還可以調(diào)節(jié)抗壞血酸-谷胱甘肽循環(huán)中非酶促抗氧化物質(zhì)的含量以及比例來加強活性氧的清除,從而緩解鹽脅迫對青綠苔草植株的傷害作用。3.外源α-生育酚改善了鹽脅迫下青綠苔草的滲透調(diào)節(jié)功能。在鹽脅迫下,青綠苔草植株體內(nèi)的K~+/Na~+、Ca~(2+)/Na~+下降;游離脯氨酸和可溶性糖含量均顯著升高,可溶性蛋白含量呈先上升后下降的趨勢。噴施α-生育酚顯著提高了鹽脅迫下青綠苔草植株體內(nèi)K~+/Na~+、Ca~(2+)/Na~+值;游離脯氨酸含量和可溶性蛋白積累量與純鹽脅迫相比顯著提高,可溶性糖含量無顯著變化。說明α-生育酚可以通過調(diào)節(jié)青綠苔草植株體內(nèi)的無機離子和有機滲透調(diào)節(jié)物質(zhì),使植物維持平衡的滲透壓和離子比例。4.外源α-生育酚可以顯著改善鹽脅迫下青綠苔草的光合特性。鹽脅迫下青綠苔草的葉綠素含量和氣孔導(dǎo)度(Gs)顯著下降,從而導(dǎo)致葉片凈光合速率(Pn)下降;鹽脅迫顯著降低了青綠苔草的PSⅡ?qū)嶋H光化學(xué)效率(φPSⅡ)、光化學(xué)淬滅系數(shù)(qP)和PSⅡ最大潛在光化學(xué)效率(Fv/Fm)。外源噴施α-生育酚提高了青綠苔草的葉綠素b和類胡蘿卜素含量,以及Gs、Pn、φPSⅡ和qP值,同時降低了胞間CO_2濃度(Ci)。說明在鹽脅迫下,青綠苔草的葉綠素PSⅡ反應(yīng)中心受到破壞,光合性能下降;外源α-生育酚可以通過增強光合電子傳遞效率,增加光化學(xué)反應(yīng)分配的光能份額,從而提高實際光化學(xué)效率,增強青綠苔草植株的耐鹽性。
[Abstract]:Soil salinization will seriously affect the growth and development of plants. Reducing the damage of plants under salt stress and improving the adaptability of plants to salt-alkali environment through the regulation of exogenous chemicals are of great significance to promote the normal growth and development of plants under salt stress and greening of saline-alkali land. In this study, Carex leucochlora was used to study the effects of different concentrations of exogenous alpha-tocopherol on growth inhibition and injury relief of Carex leucochlora under salt (0.8% NaCl) stress. The aim of this study is to reveal the main physiological regulation function of exogenous alpha-tocopherol in improving salt tolerance of Carex viridis under salt stress and to provide a theoretical basis for enhancing salt tolerance of plants in production. The results are as follows: 1. Tocopherol treatment could alleviate the damage to the growth and plasma membrane of Carex viridis under salt stress, and further increase the content of endogenous tocopherol. The content of malondialdehyde (MDA) and the relative permeability of plasma membrane decreased with the accumulation of high and dry matter, and the content of endogenous tocopherol increased further. Among them, 0.8mM exogenous alpha-tocopherol had the best mitigation effect on salt stress injury, and the content of endogenous tocopherol was the highest at this concentration. 2. Exogenous alpha-tocopherol could increase the content of endogenous tocopherol in Carex viridis. The activity of antioxidant enzymes and the improvement of ascorbic Acid-glutathione cycle in Carex viridis decreased the accumulation of excessive reactive oxygen species in plants under salt stress. The contents of ASA/DHA and GSH/GSSG increased first and then decreased, while the ratios of ASA/DHA and GSH/GSSG decreased significantly. Exogenous spraying of alpha-tocopherol increased the activities of SOD, POD and CAT, increased the contents of ASA and GSH, increased the ratios of ASA/DHA and GSH/GSSG, and increased the anti-scorbuting ability of the plants under salt stress. The activities of acid oxidase (APX), glutathione reductase (GR) and deoxyascorbate reductase (DHAR) were significantly increased. These results indicated that alpha-tocopherol could not only reduce the excessive reactive oxygen species in plants by increasing the activity of antioxidant enzymes, but also regulate the non-enzymatic antioxidants in the ascorbate-glutathione cycle under salt stress. The content and proportion of substance enhanced the scavenging of reactive oxygen species (ROS) and alleviated the damage of salt stress to Carex viridis. 3. Exogenous alpha-tocopherol improved the osmotic regulation of Carex viridis under salt stress. The content of soluble protein increased firstly and then decreased. Spraying alpha-tocopherol significantly increased K~+/Na~+, Ca~ (2+)/Na~+ values in Carex viridis plants under salt stress. Free proline content and soluble protein accumulation increased significantly compared with pure salt stress, but soluble sugar content did not change significantly. Over-regulation of inorganic ions and organic osmotic regulators in Carex viridis resulted in a balanced osmotic pressure and ion ratio. 4. Exogenous alpha-tocopherol could significantly improve the photosynthetic characteristics of Carex viridis under salt stress. Chlorophyll content and stomatal conductance (Gs) of Carex viridis significantly decreased under salt stress, resulting in a net leaf. Photosynthetic rate (Pn) decreased, salt stress significantly reduced PS II actual photochemical efficiency (phiPS II), photochemical quenching coefficient (qP) and PS II maximum potential photochemical efficiency (Fv/Fm). The concentration of O_2 (Ci) showed that the reaction center of chlorophyll PSII was destroyed and the photosynthetic performance was decreased under salt stress. Exogenous alpha-tocopherol could enhance the photosynthetic electron transfer efficiency and increase the share of light energy allocated by photochemical reaction, thereby improving the actual photochemical efficiency and enhancing the salt tolerance of the plant.
【學(xué)位授予單位】:山東農(nóng)業(yè)大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2017
【分類號】:S688.4

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