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Salicylic Acid Alleviates the Cadmium Toxicity in Barley Seedlings

机译:水杨酸减轻大麦幼苗中镉的毒性

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摘要

Salicylic acid (SA) plays a key role in plant disease resistance and hypersensitive cell death but is also implicated in hardening responses to abiotic stressors. Cadmium (Cd) exposure increased the free SA contents of barley (Hordeum vulgare) roots by a factor of about 2. Cultivation of dry barley caryopses presoaked in SA-containing solution for only 6 h or single transient addition of SA at a 0.5 mm concentration to the hydroponics solution partially protected the seedlings from Cd toxicity during the following growth period. Both SA treatments had little effect on growth in the absence of Cd, but increased root and shoot length and fresh and dry weight and inhibited lipid peroxidation in roots, as indicated by malondialdehyde contents, in the presence of Cd. To test whether this protection was due to up-regulation of antioxidant enzymes, activities and transcript levels of the H2O2-metabolizing enzymes such as catalase and ascorbate peroxidase were measured in control and SA-treated seedlings in the presence or absence of 25 μm Cd. Cd stress increased the activity of these enzymes by variable extent. SA treatments strongly or completely suppressed the Cd-induced up-regulation of the antioxidant enzyme activities. Slices from leaves treated with SA for 24 h also showed an increased level of tolerance toward high Cd concentrations as indicated by chlorophyll a fluorescence parameters. The results support the conclusion that SA alleviates Cd toxicity not at the level of antioxidant defense but by affecting other mechanisms of Cd detoxification.
机译:水杨酸(SA)在植物抗病性和超敏性细胞死亡中起关键作用,但也涉及对非生物胁迫的强化反应。镉暴露使大麦根的游离SA含量增加了约2倍。将预先浸泡在含SA溶液中的干大麦颈章鱼培养仅6 h或以0.5 mm的浓度单次添加SA在随后的生长期中,水培液的部分施用可部分保护幼苗免受Cd的毒性。两种SA处理在没有Cd的情况下对生长几乎没有影响,但是增加了根和茎的长度以及鲜重和干重,并抑制了根中丙二醛含量,表明存在Cd时根中的脂质过氧化。为了测试这种保护作用是否是由于抗氧化酶的上调所致,在有或没有25μmCd的情况下,在对照和SA处理的幼苗中测量H2O2代谢酶(例如过氧化氢酶和抗坏血酸过氧化物酶)的活性和转录水平。镉胁迫以不同程度增加了这些酶的活性。 SA处理强烈或完全抑制了Cd诱导的抗氧化酶活性的上调。叶绿素a荧光参数表明,用SA处理24 h的叶片切片对高Cd浓度的耐受性也有所提高。结果支持以下结论:SA不会在抗氧化剂防御水平上减轻Cd毒性,而是通过影响Cd解毒的其他机制来减轻Cd毒性。

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