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Zinc-Dependent Protection of Tobacco and Rice Cells From Aluminum-Induced Superoxide-Mediated Cytotoxicity.

Lin C, Hara A, Comparini D, Bouteau F, Kawano T - Front Plant Sci (2015)

Bottom Line: Earlier studies suggested that lack of zinc often results in ROS-mediated oxidative damage to plant cells.In the present study, the effect of Zn(2+) on Al(3+)-induced superoxide generation in the cell suspension cultures of tobacco (Nicotiana tabacum L., cell-line, BY-2) and rice (Oryza sativa L., cv.Obtained results indicated that presence of Zn(2+) at physiological concentrations can protect the cells by preventing the Al(3+)-induced superoxide generation and cell death.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Environmental Engineering and Graduate School of Environmental Engineering, The University of Kitakyushu , Kitakyushu, Japan.

ABSTRACT
Al(3+) toxicity in growing plants is considered as one of the major factors limiting the production of crops on acidic soils worldwide. In the last 15 years, it has been proposed that Al(3+) toxicity are mediated with distortion of the cellular signaling mechanisms such as calcium signaling pathways, and production of cytotoxic reactive oxygen species (ROS) causing oxidative damages. On the other hand, zinc is normally present in plants at high concentrations and its deficiency is one of the most widespread micronutrient deficiencies in plants. Earlier studies suggested that lack of zinc often results in ROS-mediated oxidative damage to plant cells. Previously, inhibitory action of Zn(2+) against lanthanide-induced superoxide generation in tobacco cells have been reported, suggesting that Zn(2+) interferes with the cation-induced ROS production via stimulation of NADPH oxidase. In the present study, the effect of Zn(2+) on Al(3+)-induced superoxide generation in the cell suspension cultures of tobacco (Nicotiana tabacum L., cell-line, BY-2) and rice (Oryza sativa L., cv. Nipponbare), was examined. The Zn(2+)-dependent inhibition of the Al(3+)-induced oxidative burst was observed in both model cells selected from the monocots and dicots (rice and tobacco), suggesting that this phenomenon (Al(3+)/Zn(2+) interaction) can be preserved in higher plants. Subsequently induced cell death in tobacco cells was analyzed by lethal cell staining with Evans blue. Obtained results indicated that presence of Zn(2+) at physiological concentrations can protect the cells by preventing the Al(3+)-induced superoxide generation and cell death. Furthermore, the regulation of the Ca(2+) signaling, i.e., change in the cytosolic Ca(2+) ion concentration, and the cross-talks among the elements which participate in the pathway were further explored.

No MeSH data available.


Related in: MedlinePlus

Inhibition of the Al3+-induced generation of O2•– in the presence of Zn2+. Typical records of Al3+-induced O2•– generation in the absence and the presence of ZnSO4 measured with CLA (A, tobacco; B, rice). Arrows indicate the time points for addition of AlCl3 (3 mM, tobacco; 100 mM, rice). Effects of Zn2+ concentration on Al3+-induced O2•– generation (C, tobacco; D, rice). Vertical error bars, SD; n = 3.
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Figure 3: Inhibition of the Al3+-induced generation of O2•– in the presence of Zn2+. Typical records of Al3+-induced O2•– generation in the absence and the presence of ZnSO4 measured with CLA (A, tobacco; B, rice). Arrows indicate the time points for addition of AlCl3 (3 mM, tobacco; 100 mM, rice). Effects of Zn2+ concentration on Al3+-induced O2•– generation (C, tobacco; D, rice). Vertical error bars, SD; n = 3.

Mentions: To assess the effect of Zn2+, the cells of tobacco and rice were pre-treated with various concentration of ZnSO4 for 5 min and then AlCl3 was added to the cells (Figure 3). In tobacco cell, the O2•– generation induced by 3 mM Al3+ was significantly inhibited by 1 mM or higher concentrations of Zn2+, whilst in rice cell, 0.1 mM of Zn2+ was high enough to achieve a significant inhibition of O2•– generation induced by 100 mM Al3+. Although Zn2+-dependent retardation of lanthanide-induced O2•– production has been reported (Kawano et al., 2002), the Al3+-induced oxidative burst was simply inhibited without allowing the onset of slower increase in O2•– production.


Zinc-Dependent Protection of Tobacco and Rice Cells From Aluminum-Induced Superoxide-Mediated Cytotoxicity.

Lin C, Hara A, Comparini D, Bouteau F, Kawano T - Front Plant Sci (2015)

Inhibition of the Al3+-induced generation of O2•– in the presence of Zn2+. Typical records of Al3+-induced O2•– generation in the absence and the presence of ZnSO4 measured with CLA (A, tobacco; B, rice). Arrows indicate the time points for addition of AlCl3 (3 mM, tobacco; 100 mM, rice). Effects of Zn2+ concentration on Al3+-induced O2•– generation (C, tobacco; D, rice). Vertical error bars, SD; n = 3.
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Related In: Results  -  Collection

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Figure 3: Inhibition of the Al3+-induced generation of O2•– in the presence of Zn2+. Typical records of Al3+-induced O2•– generation in the absence and the presence of ZnSO4 measured with CLA (A, tobacco; B, rice). Arrows indicate the time points for addition of AlCl3 (3 mM, tobacco; 100 mM, rice). Effects of Zn2+ concentration on Al3+-induced O2•– generation (C, tobacco; D, rice). Vertical error bars, SD; n = 3.
Mentions: To assess the effect of Zn2+, the cells of tobacco and rice were pre-treated with various concentration of ZnSO4 for 5 min and then AlCl3 was added to the cells (Figure 3). In tobacco cell, the O2•– generation induced by 3 mM Al3+ was significantly inhibited by 1 mM or higher concentrations of Zn2+, whilst in rice cell, 0.1 mM of Zn2+ was high enough to achieve a significant inhibition of O2•– generation induced by 100 mM Al3+. Although Zn2+-dependent retardation of lanthanide-induced O2•– production has been reported (Kawano et al., 2002), the Al3+-induced oxidative burst was simply inhibited without allowing the onset of slower increase in O2•– production.

Bottom Line: Earlier studies suggested that lack of zinc often results in ROS-mediated oxidative damage to plant cells.In the present study, the effect of Zn(2+) on Al(3+)-induced superoxide generation in the cell suspension cultures of tobacco (Nicotiana tabacum L., cell-line, BY-2) and rice (Oryza sativa L., cv.Obtained results indicated that presence of Zn(2+) at physiological concentrations can protect the cells by preventing the Al(3+)-induced superoxide generation and cell death.

View Article: PubMed Central - PubMed

Affiliation: Faculty of Environmental Engineering and Graduate School of Environmental Engineering, The University of Kitakyushu , Kitakyushu, Japan.

ABSTRACT
Al(3+) toxicity in growing plants is considered as one of the major factors limiting the production of crops on acidic soils worldwide. In the last 15 years, it has been proposed that Al(3+) toxicity are mediated with distortion of the cellular signaling mechanisms such as calcium signaling pathways, and production of cytotoxic reactive oxygen species (ROS) causing oxidative damages. On the other hand, zinc is normally present in plants at high concentrations and its deficiency is one of the most widespread micronutrient deficiencies in plants. Earlier studies suggested that lack of zinc often results in ROS-mediated oxidative damage to plant cells. Previously, inhibitory action of Zn(2+) against lanthanide-induced superoxide generation in tobacco cells have been reported, suggesting that Zn(2+) interferes with the cation-induced ROS production via stimulation of NADPH oxidase. In the present study, the effect of Zn(2+) on Al(3+)-induced superoxide generation in the cell suspension cultures of tobacco (Nicotiana tabacum L., cell-line, BY-2) and rice (Oryza sativa L., cv. Nipponbare), was examined. The Zn(2+)-dependent inhibition of the Al(3+)-induced oxidative burst was observed in both model cells selected from the monocots and dicots (rice and tobacco), suggesting that this phenomenon (Al(3+)/Zn(2+) interaction) can be preserved in higher plants. Subsequently induced cell death in tobacco cells was analyzed by lethal cell staining with Evans blue. Obtained results indicated that presence of Zn(2+) at physiological concentrations can protect the cells by preventing the Al(3+)-induced superoxide generation and cell death. Furthermore, the regulation of the Ca(2+) signaling, i.e., change in the cytosolic Ca(2+) ion concentration, and the cross-talks among the elements which participate in the pathway were further explored.

No MeSH data available.


Related in: MedlinePlus