An intracellular mechanism of aluminum tolerance associated with high antioxidant status in cultured tobacco cells
An intracellular mechanism of aluminum tolerance associated with high antioxidant status in cultured tobacco cells
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DOI：
10.1016/s0162-0134(03)00182-x
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发表时间：
2003-09-15
影响因子：
3.9
通讯作者：
Matsumoto, H
中科院分区：
文献类型：
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作者：
Devi, SR;Yamamoto, Y;Matsumoto, H
在烟草耐铝细胞系 (ALT301) 和亲本铝敏感细胞系 (SL) 中研究了铝 (Al) 耐受机制以及氧化应激耐受性。在简单的钙溶液中暴露 24 It 的铝期间，铝引发了 SL 中活性氧 (ROS) 的演化，其含量远高于 ALT301 [植物生理学。 128（2002）63]。在该条件下，Al将两种细胞系的柠檬酸分泌率提高到相同程度。 Al 增强了两种细胞系中锰超氧化物歧化酶 (MnSOD) 的基因表达，但在 SL 中的表达率显着高于 ALT301，并且还将两种细胞系中 MnSOD 的酶活性增强到几乎相同的水平。这些结果表明Al与有机酸和MnSOD的细胞外螯合不参与ALT301的Al耐受机制。在正常生长条件下，ALT301 含有的抗坏血酸 (ASA) 和谷胱甘肽 (GSH) 水平高于 SL。在生长培养基中铝处理后培养 24 小时期间，但在简单 Ca2+ 溶液中暴露 24 小时期间，SL 中的脂质过氧化增强程度远高于 ALT301，并且与 ALT301 相比，ASA 和 GSH 的平均 SL 量被耗尽。 Al 处理前预先加载 ASA 可改善 Al 处理后培养过程中 SL 的生长。 ALT301 还表现出对 H2O2、Fe2+ 和 Cu2+ 的交叉耐受性。在这些氧化剂暴露下，与 SL 相比，ALT301 含有较低水平的细胞内 H2O2 或脂质过氧化物，并保持较高含量的 ASA 和 GSH。综上所述，我们得出结论，细胞中铝的积累仅在生长条件下增强脂质过氧化，并且 ALT301 中 ASA 和 GSH 的含量比 SL 中更高，这似乎是 ALT301 对铝的耐受机制的部分原因，通过保护细胞免受铝或其他氧化剂通常增强的脂质过氧化或 H2O2 的影响。 (C) 2003 Elsevier Inc. 保留所有权利。
An aluminum (Al) tolerance mechanism, together with oxidative stress tolerance, was investigated in an Al tolerant cell line (ALT301) and the parental Al sensitive cell line (SL) of tobacco. During Al exposure in a simple calcium solution for 24 It, Al triggered the evolution of a reactive oxygen species (ROS) in SL much higher than ALT301 [Plant Physiol. 128 (2002) 63]. Under the conditions, Al enhanced comparable rates of citrate secretion from both cell lines to the same extent. Al enhanced the gene expression of manganese superoxide dismutase (MnSOD) in both cell lines, but at a significantly higher rate in SL than in ALT301, and also enhanced the enzyme activity of MnSOD in both cell lines to nearly the same level. These results suggest that the extracellular chelation of Al with organic acids and MnSOD is not involved in the mechanism of Al tolerance of ALT301. ALT301 contained ascorbate (ASA) and glutathione (GSH) levels that were higher than SL under normal growth conditions. During 24 h of post-Al treatment culture in growth medium, but not during 24-h Al exposure in a simple Ca2+ Solution, lipid peroxidation was enhanced in SL much higher than in ALT301, and the average SL amounts of ASA and GSH were exhausted compared to ALT301. Pre-loading of ASA prior to Al treatment improved the growth of SL during the post-Al treatment culture. ALT301 also exhibited cross-tolerance to H2O2, Fe2+ and Cu2+. Under these oxidant exposures, ALT301 contained lower levels of intracellular H2O2 or lipid peroxides, and maintained higher amounts of ASA and GSH than SL. Taken together, we conclude that the accumulation of Al in cells enhances the peroxidation of lipids exclusively under growing conditions, and that the higher content of ASA and GSH in ALT301 than in SL seems to be in part responsible for the tolerance mechanism of ALT301 to Al by protecting cells from either lipid peroxidation or H2O2 commonly enhanced by Al or other oxidants. (C) 2003 Elsevier Inc. All rights reserved.