IAA对Cd^(2+)胁迫下拟南芥渗透调节物质及抗氧化特性的影响

Effect of IAA on the osmotic adjustment substance and antioxidant properties in Arabidopsis thalian aseedlings under Cd^(2+) stress

以拟南芥为供试植物,采用室内基质培养的方法,研究IAA处理对植株镉胁迫生理的影响,实验共设对照组、1μmol·L^(-1) IAA处理组、100mg·L^(-1) CdCl_2处理组、1μmol·L^(-1) IAA+100mg·L^(-1) CdCl_2处理组.结果表明:随Cd^(2+)胁迫时间延长,CdCl_2处理组中游离脯氨酸、可溶性蛋白、可溶性糖含量显著增加,IAA+CdCl_2处理组游离脯氨酸等渗透调节物质含量与CdCl_2处理组相比分别增加了18.01%~28.15%、24.8%~19.2%和3.3%~11.6%(p<0.05);CdCl_2处理组MDA含量显著升高,IAA+CdCl_2处理组MDA含量与CdCl_2处理组相比降低了7.1%~12.39%(p<0.05);CdCl_2处理组中SOD、POD、CAT活性增加但明显低于对照组,IAA+CdCl_2处理组SOD等抗氧化酶活性与CdCl_2处理组相比分别增加了10%~4.35%、9.3%~7.04%与20.97%~24.6%(p<0.05).表明IAA处理可以通过提高拟南芥体内渗透调节物质含量及抗氧化酶活性来清除氧自由基,维持细胞膜结构的稳定性,并降低膜脂过氧化伤害程度,从而缓解Cd^(2+)对拟南芥生长的毒害作用.

Abstract： Effects of auxin（lAA）pretreatment of physiological responses on cadmium stress were investigated, taking Arabidopsis thaliana as the test plant and cultivating indoor. Test plants were comprised of control group,1μmol·L^-1 IAA group, 100 mg·L^-1 CdCl2 stress group and cadmium stress on 1 μmol·L^-1 IAA group.The results showed that the contents of free proline, soluble sugar and soluble protein in CdCl2 pretreatment group increased significantly with the pro longation of CdCl2 stress and extension of time. In IAA ＋ CdCl2 pretreatment group, the contents of free proline, soluble sugar and soluble protein significantly increased by 1 8.0 1%-28.1 5% and 24.8 %-1 9.2% and 3.3%- 1 1.6% （p〈0.05）, respectively. Moreover, cadmium stress induced high levels of maIondiaIdehyde （MDA）, while IAA pretreatment decreased the contents of MDA by 7.1%-1 2.39%, under cadmium conditions. In addition, the activities of SOD, POD and CAT were significantly respectively increased by 10%-4.35%, 9.3%-7.04% and 20.97%-24.6%（p〈0.05） in lAA pretreatment group. It stlggested effects of Cd^2＋ stress oi1 Arabidopsis thaliana were mitigated by applying IAA through increasing the con tents of osmotic adjustment substances in Arabidopsis thaliana and increasing the activities of the antioxidant enzymes to alle viate the damage from peroxidation of membrane lipid.