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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

Al3+-induced cell death and its inhibition by addition of Zn2+ in tobacco BY-2 cells. (A) Effect of AlCl3 concentration on cell death induction. Cell death was assessed by Evans blue staining 8 h after addition of AlCl3. (B) Effect of post-Al3+ incubation (0.5–8 h) on development of cell death. (C) Effect of ZnSO4 on Al3+-induced cell death. Cell death was assessed 6 h after Al3+ treatments. Vertical error bars, SD; n = 3.
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Figure 6: Al3+-induced cell death and its inhibition by addition of Zn2+ in tobacco BY-2 cells. (A) Effect of AlCl3 concentration on cell death induction. Cell death was assessed by Evans blue staining 8 h after addition of AlCl3. (B) Effect of post-Al3+ incubation (0.5–8 h) on development of cell death. (C) Effect of ZnSO4 on Al3+-induced cell death. Cell death was assessed 6 h after Al3+ treatments. Vertical error bars, SD; n = 3.

Mentions: As shown in Figures 6A,B, treatment of tobacco BY-2 cells with various concentrations of AlCl3 resulted in cell death induction. Notably, the presence of Zn2+ significantly protected the cells from the induction of cell death by Al3+ (Figure 6C), as predicted by the action of Zn2+ against Al3+-induced oxidative burst.


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)

Al3+-induced cell death and its inhibition by addition of Zn2+ in tobacco BY-2 cells. (A) Effect of AlCl3 concentration on cell death induction. Cell death was assessed by Evans blue staining 8 h after addition of AlCl3. (B) Effect of post-Al3+ incubation (0.5–8 h) on development of cell death. (C) Effect of ZnSO4 on Al3+-induced cell death. Cell death was assessed 6 h after Al3+ treatments. Vertical error bars, SD; n = 3.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664629&req=5

Figure 6: Al3+-induced cell death and its inhibition by addition of Zn2+ in tobacco BY-2 cells. (A) Effect of AlCl3 concentration on cell death induction. Cell death was assessed by Evans blue staining 8 h after addition of AlCl3. (B) Effect of post-Al3+ incubation (0.5–8 h) on development of cell death. (C) Effect of ZnSO4 on Al3+-induced cell death. Cell death was assessed 6 h after Al3+ treatments. Vertical error bars, SD; n = 3.
Mentions: As shown in Figures 6A,B, treatment of tobacco BY-2 cells with various concentrations of AlCl3 resulted in cell death induction. Notably, the presence of Zn2+ significantly protected the cells from the induction of cell death by Al3+ (Figure 6C), as predicted by the action of Zn2+ against Al3+-induced oxidative burst.

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