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.

探索内源脱落酸（ABA）的功能，以应对过量的锌（Zn），拟南芥（Arabidopsis thaliana）突变株的愈伤组织，abi1-1（对ABA不敏感）和aba1-1（ABA含量降低），以及使用了它们相关的野生型（Landsberg erecta，Ler）。过量的锌导致氧化损伤，其特征在于离子泄漏，丙二醛（MDA）和过氧化氢（H ₂ O ₂）积累，以及拟南芥愈伤组织中相对细胞活力降低。与野生型（Ler）相比，缺乏ABA的突变体（aba-1）的愈伤组织遭受更严重的氧化损伤。）愈伤组织。钨酸钠是一种ABA合成抑制剂，加剧了过量的Zn诱导的离子泄漏，H ₂ O ₂和MDA在野生型和aba1-1突变体愈伤组织中的积累。同样，钨酸钠明显抑制脯氨酸的产生和抗坏血酸过氧化物酶（APX）的活性，而在过量锌的存在下，野生型和aba1-1突变体愈伤组织中脂氧合酶（LOX）活性得到增强。相反，外源ABA处理显着提高了脯氨酸的浓度和APX活性，并抑制了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的积累，并降低了野生型和aba-1的相对细胞活力。突变体愈伤组织。此外，在过量的锌下，未观察到钨酸钠或外源ABA对源自abi1-1突变体的愈伤组织的显着影响。内源性ABA可能在兴奋性抗氧化酶和脯氨酸积累中起信号作用，因此可以防止因过量Zn引起的毒性。