酸盐诱导的AHb1表达加剧了植物中的Cd毒性
Yun Wang1, Bingfang Luo2, Siyu Zhang3
1Planting Technology Extension Center of Dongyang, Jinhua 322100, China.
Journal of hazardous materials
|September 10, 2023
概括
的供应会影响植物中的毒性. 过度表达血红蛋白基因Hb1通过抑制氧化的产生,从而导致氧化应激,在酸盐条件下增加了的毒性.
科学领域:
- 植物生物学 植物生物学
- 环境毒理学环境毒理学
- 分子机制的分子机制
背景情况:
- (Cd) 对植物具有显著的毒性,但抵抗机制,特别是有关 (N) 供应的机制,尚未完全理解.
- 非共生血红蛋白基因Hb1参与植物中的氧化 (NO) 清理.
研究的目的:
- 为了研究Hb1基因在不同源下对植物耐药性的作用.
- 阐明关联代谢,Hb1表达和毒性的分子机制.
主要方法:
- 在不同的条件下 (NH4+-N和NO3--N) 和Cd暴露下对野生型 (WT),AHb1-过度表达 (H7) 和AHb1-沉默 (L3) 植物进行比较分析.
- 评估植物生物质,Cd度,过氧化 (H2O2) 积累和氧化损伤.
- 应用NO捐赠剂来评估其对Cd诱导的压力的影响.
主要成果:
- 在NH4+-N下,无论Hb1表达如何,Cd对植物生物质没有差异性影响.
- 在NO3--N下,Cd在L3植物中引起的生物质压力较小,而在H7植物中引起的压力较大,与WT植物相比,Cd耐受性指数为L3>WT>H7.
- Cd吸收不受Hb1表达水平的影响. 在H7植物中,Cd暴露增加了H2O2的积累和氧化损伤,而NO的供体应用反转了这种情况.
结论:
- 酸盐诱导的Hb1表达抑制了Cd诱导的NO生产,导致活性氧物种 (ROS) 爆发增加,并加剧了Cd毒性.
- Hb1在调节植物对Cd毒性的反应中起着至关重要的作用,特别是在富含酸盐的条件下.
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