The role of ABA in the responses of wild-type and abscisic acid mutants of Arabidopsis thaliana to excess zinc

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.