Devi S Rama, Yamamoto Yoko, Matsumoto Hideaki
Research Institute for Bioresources, Okayama University, Kurashiki, Chuo 710-0046, Japan.
J Inorg Biochem. 2003 Sep 15;97(1):59-68. doi: 10.1016/s0162-0134(03)00182-x.
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 h, 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 Ca(2+) 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 H(2)O(2), Fe(2+) and Cu(2+). Under these oxidant exposures, ALT301 contained lower levels of intracellular H(2)O(2) 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 H(2)O(2) commonly enhanced by Al or other oxidants.
在烟草的耐铝细胞系（ALT301）及其亲本铝敏感细胞系（SL）中研究了铝（Al）耐受机制以及氧化应激耐受性。在简单钙溶液中铝暴露24小时期间，铝引发的活性氧（ROS）在SL中的释放量远高于ALT301[《植物生理学》128（2002）63]。在此条件下，铝使两个细胞系中柠檬酸的分泌速率提高到相同程度。铝增强了两个细胞系中锰超氧化物歧化酶（MnSOD）的基因表达，但在SL中的增强速率显著高于ALT301，并且也使两个细胞系中MnSOD的酶活性提高到几乎相同水平。这些结果表明，铝与有机酸和MnSOD的细胞外螯合不参与ALT301的耐铝机制。在正常生长条件下，ALT301中抗坏血酸（ASA）和谷胱甘肽（GSH）的含量高于SL。在生长培养基中进行铝处理后24小时的培养期间，但不是在简单Ca(2+)溶液中24小时铝暴露期间，SL中的脂质过氧化增强程度远高于ALT301，并且与ALT301相比，SL中ASA和GSH的平均含量耗尽。在铝处理之前预先加载ASA可改善铝处理后培养期间SL的生长。ALT301对H(2)O(2)、Fe(2+)和Cu(2+)也表现出交叉耐受性。在这些氧化剂暴露下，ALT301中细胞内H(2)O(2)或脂质过氧化物的含量较低，并且比SL维持更高含量的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的含量高于SL似乎部分负责ALT301对铝的耐受机制，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H(2)O(2)的影响。
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