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首页> 外文期刊>Acta Physiologiae Plantarum >The role of ABA in the responses of wild-type and abscisic acid mutants of Arabidopsis thaliana to excess zinc
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The role of ABA in the responses of wild-type and abscisic acid mutants of Arabidopsis thaliana to excess zinc

机译:ABA在拟南芥野生型和脱落酸突变体对多余锌的反应中的作用

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To explore the function of endogenous abscisic acid (ABA) in answer to excess zinc (Zn), calli from Arabidopsis (Arabidopsis thaliana) mutant lines, abi1-1 (ABA insensitive) and aba1-1 (with reduced level of ABA), and their associated wild-type (Landsberg erecta, Ler) were used. Excess Zn resulted in oxidative damage characterized by ion leakage, malondialdehyde (MDA), and hydrogen peroxide (H2O2) accumulation, and relative cell viability decrease in Arabidopsis calli. ABA-deficient mutant (aba-1) callus suffered more serious oxidative damage in comparison with wild-type (Ler) callus. Sodium tungstate, an ABA synthesis inhibitor, aggravated excess Zn-induced ion leakage, H2O2 and MDA accumulation in wild-type and aba1-1 mutant calli. Also, sodium tungstate obviously suppressed proline production and ascorbate peroxidase (APX) activity whereas promoted lipoxygenase (LOX) activity in wild-type and aba1-1 mutant calli in the presence of excess Zn. Instead, exogenous ABA treatment significantly elevated proline concentration and APX activity and inhibited LOX activity and thus alleviated excess Zn-induced ion leakage, H2O2 and MDA accumulation, and relative cell viability decrease in wild-type and aba-1 mutant calli. Moreover, no significant effects of sodium tungstate or exogenous ABA application on calli derived from abi1-1 mutant were observed under excess Zn. Endogenous ABA might function as a signal in exciting antioxidases and proline accumulation and thus protect against toxicity induced by excess Zn.
机译:探讨内源性脱落酸(ABA)答案的答案到过量锌(Zn),来自拟南芥(拟南芥)突变线,ABI1-1(ABA不敏感)和ABA1-1(ABA水平降低)的他们使用了他们相关的野生型(Landsberg Eerecta,Ler)。过量的Zn导致由离子泄漏,丙二醛(MDA)和过氧化氢(H2O2)积累的氧化损伤,以及拟南芥Calli的相对细胞活力减少。与野生型(LER)愈伤组织相比,ABA缺陷型突变体(ABA-1)愈伤组织遭受更严重的氧化损伤。钨酸钠,ABA合成抑制剂,加重过量的Zn诱导的离子泄漏,H2O2和MDA在野生型和ABA1-1突变疾病中积累。此外,钨酸钠明显抑制了脯氨酸产量和抗坏血酸过氧化物酶(APX)活性,而在过量Zn存在下促进野生型和ABA1-1突变疾病中的脂氧合酶(LOX)活性。相反,外源性ABA治疗显着升高了脯氨酸浓度和APX活性,抑制了LOX活性,从而减轻了过量的Zn诱导的离子泄漏,H 2 O 2和MDA积聚,以及野生型和ABA-1突变疾病中的相对细胞活力降低。此外,在过量的Zn下观察到在过量的Zn下观察到碳酮钠或外源ABA应用衍生自ABI1-1突变体的愈伤组织。内源性ABA可能用作激发抗氧化酶和脯氨酸积累中的信号,从而防止过量Zn诱导的毒性。

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