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过氧化物酶体缺陷的烟草叶片在百草枯胁迫下活性氧的形成和细胞死亡。

Reactive oxygen species formation and cell death in catalase-deficient tobacco leaf discs exposed to paraquat.

机构信息

Departamento de Química Biológica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956, 1113 Buenos Aires, Argentina.

出版信息

Biol Trace Elem Res. 2012 May;146(2):246-55. doi: 10.1007/s12011-011-9244-1. Epub 2011 Nov 19.

Abstract

In the present work, the response of tobacco (Nicotiana tabaccum L.) wild-type SR1 and transgenic CAT1AS plants (with a basal reduced CAT activity) was evaluated after exposure to the herbicide paraquat (PQ). Superoxide anion (O (2) (.-) ) formation was inhibited at 3 or 21 h of exposure, but H(2)O(2) production and ion leakage increased significantly, both in SR1 or CAT1AS leaf discs. NADPH oxidase activity was constitutively 57% lower in non-treated transgenic leaves than in SR1 leaves and was greatly reduced both at 3 or 21 h of PQ treatment. Superoxide dismutase (SOD) activity was significantly reduced by PQ after 21 h, showing a decrease from 70% to 55%, whereas catalase (CAT) activity decreased an average of 50% after 3 h of treatment, and of 90% after 21 h, in SR1 and CAT1AS, respectively. Concomitantly, total CAT protein content was shown to be reduced in non-treated CAT1AS plants compared to control SR1 leaf discs at both exposure times. PQ decreased CAT expression in SR1 or CAT1AS plants at 3 and 21 h of treatment. The mechanisms underlying PQ-induced cell death were possibly not related exclusively to ROS formation and oxidative stress in tobacco wild-type or transgenic plants.

摘要

在本工作中,评价了接触除草剂百草枯(PQ)后烟草(Nicotiana tabaccum L.)野生型 SR1 和转基因 CAT1AS 植株(基础 CAT 活性降低)的反应。在 3 或 21 小时暴露时,超氧阴离子(O2(-))的形成受到抑制,但在 SR1 或 CAT1AS 叶片圆盘,H2O2 的产生和离子漏出明显增加。与 SR1 叶片相比,未经处理的转基因叶片中的 NADPH 氧化酶活性一直低 57%,在 PQ 处理 3 或 21 小时后大大降低。在 21 小时时,超氧化物歧化酶(SOD)活性因 PQ 而显著降低,从 70%降至 55%,而 CAT 活性在 3 小时处理后平均降低 50%,在 21 小时后降低 90%,在 SR1 和 CAT1AS 中分别降低。同时,在两个暴露时间,与对照 SR1 叶片圆盘相比,未经处理的 CAT1AS 植物中的总 CAT 蛋白含量降低。在 3 和 21 小时的处理中,PQ 降低了 SR1 或 CAT1AS 植物中的 CAT 表达。PQ 诱导的细胞死亡的机制可能不仅仅与 ROS 的形成和烟草野生型或转基因植物中的氧化应激有关。

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