《植物生理学报》 2014, 50(10): 1593-1600

双氯芬酸对烟草BY-2细胞呼吸代谢的影响

刘玉亭¹, 程丹丹², 刘美君¹, 高辉远^1,*

¹山东农业大学生命科学学院, 作物生物学国家重点实验室, 山东泰安271018; ²东北林业大学生命科学学院, 哈尔滨150040

通信作者：高辉远；E-mail: gaohy@sdau.edu.cn；Tel: 0538-8245985

摘　要：

双氯芬酸是一种新的全球性环境污染物, 严重影响植物的生长发育, 但其作用机制至今尚不清楚。本研究从双氯芬酸对烟草BY-2细胞呼吸代谢和活性氧代谢的影响入手, 探讨双氯芬酸抑制植物细胞生长的作用机理。结果表明, 双氯芬酸处理1 d后, 显著抑制了烟草BY-2细胞的生长, 引起细胞内活性氧(ROS)的爆发和积累, 并导致烟草BY-2细胞死亡。双氯芬酸对烟草BY-2细胞的糖酵解途径(EMP)、三羧酸循环(TCA)和戊糖磷酸途径(PPP)三个碳代谢途径以及细胞色素氧化酶(COX)和交替氧化酶(AOX)参与的两条呼吸电子传递途径均有即时抑制作用。双氯芬酸可能通过抑制细胞线粒体呼吸电子传递链的活性, 导致电子从呼吸链泄漏加速ROS的形成, 并反馈抑制呼吸碳代谢途径, 进而导致细胞内物质代谢和能量代谢紊乱, 这些是双氯芬酸抑制烟草BY-2细胞生长、导致细胞死亡的重要原因。

关键词：双氯芬酸; 烟草BY-2细胞; 呼吸代谢; 活性氧代谢; 呼吸电子传递链

收稿：2014-08-01   修定：2014-08-18

资助：高等学校博士学科点专项科研基金项目(20113702110008)和国家自然科学基金(31370276)。

Effect of Diclofenac on Respiratory Metabolism of Tobacco BY-2 Cell

LIU Yu-Ting¹, CHENG Dan-Dan², LIU Mei-Jun¹, GAO Hui-Yuan^1,*

¹State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai’an, Shandong 271018, China; ²College of Life Sciences, Northeast Forest University, Harbin 150040, China

Corresponding author: GAO Hui-Yuan; E-mail: gaohy@sdau.edu.cn; Tel: 0538-8245985

Abstract:

Diclofenac is a new kind of global environmental pollutant, influencing the growth and development of plants seriously. However, it has not been elucidated the mechanism by which the diclofenac inhibits plant growth. In order to explore the inhibition mechanism, in this study, we explored the effect of diclofenac on respiratory metabolism and metabolism of reactive oxygen species (ROS) in tobacco BY-2 cells. The results showed that after treated with diclofenac for 1 d, the growth of tobacco BY-2 cell was significantly inhibited, a burst and overproduction of ROS in the BY-2 cell were induced, which promoted death of the BY-2 cells. Diclofenac treatment instantly inhibited the respiration of the BY-2 cell, the EMP, TCA, PPP respiration pathway and the respiratory electron transport via COX and AOX were inhibited by the diclofenac treatment. Diclofenac might inhibit respiratory electron transport and the inhibition of mitochondrial respiratory electron transport chain caused electrons leaking from respiratory electron transport chain, which accelerated generation of ROS, and the inhibition of respiratory electron transport also caused feedback inhibition of respiratory carbon metabolic pathways, disordering substance metabolism and energy metabolism in the BY-2 cell, this is one of the important reasons of diclofenac to inhibit the growth and induce death of the BY-2 cells.

Key words: diclofenac; tobacco BY-2 cell; respiratory metabolism; active oxygen metabolism; respiratory electron transport chain