MOE Key Laboratory of Environment Remediation and Ecological Health, College of Environmental & Resource Sciences, Zhejiang University, Hangzhou 310058, China.
MOE Key Laboratory of Environment Remediation and Ecological Health, College of Environmental & Resource Sciences, Zhejiang University, Hangzhou 310058, China.
J Hazard Mater. 2023 Feb 5;443(Pt A):130142. doi: 10.1016/j.jhazmat.2022.130142. Epub 2022 Oct 7.
Lipid peroxidation is a primary event in plant roots exposed to aluminum (Al) toxicity, which leads to the formation of reactive aldehydes. Current evidence demonstrates that the resultant aldehydes are integrated components of cellular damage in plants. Here, we investigated the roles of aldehydes in mediating Al-induced damage, particularly cell death, using two wheat genotypes with different Al resistances. Aluminum treatment significantly induced cell death, which was accompanied by decreased root activity and cell length. Al-induced cell death displayed granular nuclei and internucleosomal fragmentation of nuclear DNA, suggesting these cells underwent programmed cell death (PCD). During this process, caspase-3-like protease activity was extensively enhanced and showed a significant difference between these two wheat genotypes. Further experiments showed that Al-induced cell death was positively correlated with aldehydes levels. Al-induced representative diagnostic markers for PCD, such as TUNEL-positive nuclei and DNA fragmentation, were further enhanced by the aldehyde donor (E)-2-hexenal, but significantly suppressed by the aldehyde scavenger carnosine. As the crucial executioner of Al-induced PCD, the activity of caspase-3-like protease was further enhanced by (E)-2-hexenal but inhibited by carnosine in wheat roots. These results suggest that reactive aldehydes sourced from lipid peroxidation mediate Al-initiated PCD probably through activating caspase-3-like protease in wheat roots.
脂质过氧化作用是植物根系暴露于铝（Al）毒性下的一个主要事件，这导致了活性醛的形成。目前的证据表明，由此产生的醛是植物细胞损伤的组成部分。在这里，我们使用两种具有不同耐铝性的小麦基因型来研究醛在介导铝诱导损伤中的作用，特别是细胞死亡。铝处理显著诱导细胞死亡，伴随着根活力和细胞长度的降低。铝诱导的细胞死亡表现出颗粒状核和核 DNA 的核小体片段化，表明这些细胞经历了程序性细胞死亡（PCD）。在此过程中，半胱天冬酶-3 样蛋白酶活性广泛增强，并且在这两种小麦基因型之间存在显著差异。进一步的实验表明，铝诱导的细胞死亡与醛水平呈正相关。铝诱导的 PCD 的代表性诊断标志物，如 TUNEL 阳性核和 DNA 片段化，通过醛供体（E）-2-己烯醛进一步增强，但被醛清除剂肌肽显著抑制。作为铝诱导的 PCD 的关键执行者，半胱天冬酶-3 样蛋白酶的活性在小麦根系中通过（E）-2-己烯醛进一步增强，但被肌肽抑制。这些结果表明，源自脂质过氧化的活性醛通过在小麦根系中激活半胱天冬酶-3 样蛋白酶来介导铝引发的 PCD。
