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Cell viability in the cadmium-stressed cell suspension cultures of tobacco is regulated by extracellular ATP, possibly by a reactive oxygen species-associated mechanism

Zhenzhen SHI, Jiaxin CAO, Hailong PANG, Lingyun JIA, Kun SUN, Hanqing FENG*

College of Life Science, Northwest Normal University, Lanzhou, 730070, China

* Address correspondence to: Hanqing Feng, email

BIOCELL 2020, 44(1), 89-99. https://doi.org/10.32604/biocell.2020.08059

Abstract

Cadmium (Cd) is one of the most widespread and toxic heavy metals to plants. Extracellular ATP (exATP) is thought to be an extracellular effector in regulating the physiological responses of plant cells to environmental stresses. However, the function of exATP in Cd-stressed plant cells is much unknown. The present work showed that treating tobacco (Nicotiana tabacum L. cv. Bright Yellow-2) cell-suspension cultures with exogenous CdCl2 reduced the cell viability, exATP level, and Mg content. However, the production of reactive oxygen species (ROS), Cd content, and electrolyte leakage of the cells were enhanced by exogenous CdCl2. When the Cd-induced accumulation of ROS was decreased by the supplement with DMTU (dimethylthiourea, a scavenger of ROS), the Cd-induced increases of the electrolyte leakage and Cd content were alleviated, and the Cd-induced reductions of cell viability were partly rescued, suggesting that Cd-induced reduction of cell viability could be related to the ROS accumulation. Under the condition of Cd stress, when the reduction of exATP level was partly rescued by exogenous ATP (20 μM), the increases of ROS production, electrolyte leakage, and Cd content were attenuated, and the reduction of cell viability was also alleviated. These observations indicate that exATP can regulate the cell viability in the Cd–stressed plant cells possibly by an ROSassociated mechanism.

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SHI,, Z. (2020). Cell viability in the cadmium-stressed cell suspension cultures of tobacco is regulated by extracellular ATP, possibly by a reactive oxygen species-associated mechanism. BIOCELL, 44(1), 89–99. https://doi.org/10.32604/biocell.2020.08059

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