Abstract
An aluminum (Al) tolerance mechanism, together with oxidative stress tolerance, was investigated in an Al tolerant cell line (ALT301) and the parental Al sensitive cell line (SL) of tobacco. During Al exposure in a simple calcium solution for 24 h, Al triggered the evolution of a reactive oxygen species (ROS) in SL much higher than ALT301 [Plant Physiol. 128 (2002) 63]. Under the conditions, Al enhanced comparable rates of citrate secretion from both cell lines to the same extent. Al enhanced the gene expression of manganese superoxide dismutase (MnSOD) in both cell lines, but at a significantly higher rate in SL than in ALT301, and also enhanced the enzyme activity of MnSOD in both cell lines to nearly the same level. These results suggest that the extracellular chelation of Al with organic acids and MnSOD is not involved in the mechanism of Al tolerance of ALT301. ALT301 contained ascorbate (ASA) and glutathione (GSH) levels that were higher than SL under normal growth conditions. During 24 h of post-Al treatment culture in growth medium, but not during 24-h Al exposure in a simple Ca2+ solution, lipid peroxidation was enhanced in SL much higher than in ALT301, and the average SL amounts of ASA and GSH were exhausted compared to ALT301. Pre-loading of ASA prior to Al treatment improved the growth of SL during the post-Al treatment culture. ALT301 also exhibited cross-tolerance to H 2O2, Fe2+ and Cu2+. Under these oxidant exposures, ALT301 contained lower levels of intracellular H 2O2 or lipid peroxides, and maintained higher amounts of ASA and GSH than SL. Taken together, we conclude that the accumulation of Al in cells enhances the peroxidation of lipids exclusively under growing conditions, and that the higher content of ASA and GSH in ALT301 than in SL seems to be in part responsible for the tolerance mechanism of ALT301 to Al by protecting cells from either lipid peroxidation or H2O2 commonly enhanced by Al or other oxidants.
| Original language | English |
|---|---|
| Pages (from-to) | 59-68 |
| Number of pages | 10 |
| Journal | Journal of Inorganic Biochemistry |
| Volume | 97 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Sep 15 2003 |
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Keywords
- Aluminum tolerance
- Ascorbic acid
- Glutathione
- Oxidative stress
- Tobacco cells
ASJC Scopus subject areas
- Biochemistry
- Inorganic Chemistry
Cite this
An intracellular mechanism of aluminum tolerance associated with high antioxidant status in cultured tobacco cells. / Devi, S. Rama; Yamamoto, Yoko; Matsumoto, Hideaki.
In: Journal of Inorganic Biochemistry, Vol. 97, No. 1, 15.09.2003, p. 59-68.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - An intracellular mechanism of aluminum tolerance associated with high antioxidant status in cultured tobacco cells
AU - Devi, S. Rama
AU - Yamamoto, Yoko
AU - Matsumoto, Hideaki
PY - 2003/9/15
Y1 - 2003/9/15
N2 - An aluminum (Al) tolerance mechanism, together with oxidative stress tolerance, was investigated in an Al tolerant cell line (ALT301) and the parental Al sensitive cell line (SL) of tobacco. During Al exposure in a simple calcium solution for 24 h, Al triggered the evolution of a reactive oxygen species (ROS) in SL much higher than ALT301 [Plant Physiol. 128 (2002) 63]. Under the conditions, Al enhanced comparable rates of citrate secretion from both cell lines to the same extent. Al enhanced the gene expression of manganese superoxide dismutase (MnSOD) in both cell lines, but at a significantly higher rate in SL than in ALT301, and also enhanced the enzyme activity of MnSOD in both cell lines to nearly the same level. These results suggest that the extracellular chelation of Al with organic acids and MnSOD is not involved in the mechanism of Al tolerance of ALT301. ALT301 contained ascorbate (ASA) and glutathione (GSH) levels that were higher than SL under normal growth conditions. During 24 h of post-Al treatment culture in growth medium, but not during 24-h Al exposure in a simple Ca2+ solution, lipid peroxidation was enhanced in SL much higher than in ALT301, and the average SL amounts of ASA and GSH were exhausted compared to ALT301. Pre-loading of ASA prior to Al treatment improved the growth of SL during the post-Al treatment culture. ALT301 also exhibited cross-tolerance to H 2O2, Fe2+ and Cu2+. Under these oxidant exposures, ALT301 contained lower levels of intracellular H 2O2 or lipid peroxides, and maintained higher amounts of ASA and GSH than SL. Taken together, we conclude that the accumulation of Al in cells enhances the peroxidation of lipids exclusively under growing conditions, and that the higher content of ASA and GSH in ALT301 than in SL seems to be in part responsible for the tolerance mechanism of ALT301 to Al by protecting cells from either lipid peroxidation or H2O2 commonly enhanced by Al or other oxidants.
AB - An aluminum (Al) tolerance mechanism, together with oxidative stress tolerance, was investigated in an Al tolerant cell line (ALT301) and the parental Al sensitive cell line (SL) of tobacco. During Al exposure in a simple calcium solution for 24 h, Al triggered the evolution of a reactive oxygen species (ROS) in SL much higher than ALT301 [Plant Physiol. 128 (2002) 63]. Under the conditions, Al enhanced comparable rates of citrate secretion from both cell lines to the same extent. Al enhanced the gene expression of manganese superoxide dismutase (MnSOD) in both cell lines, but at a significantly higher rate in SL than in ALT301, and also enhanced the enzyme activity of MnSOD in both cell lines to nearly the same level. These results suggest that the extracellular chelation of Al with organic acids and MnSOD is not involved in the mechanism of Al tolerance of ALT301. ALT301 contained ascorbate (ASA) and glutathione (GSH) levels that were higher than SL under normal growth conditions. During 24 h of post-Al treatment culture in growth medium, but not during 24-h Al exposure in a simple Ca2+ solution, lipid peroxidation was enhanced in SL much higher than in ALT301, and the average SL amounts of ASA and GSH were exhausted compared to ALT301. Pre-loading of ASA prior to Al treatment improved the growth of SL during the post-Al treatment culture. ALT301 also exhibited cross-tolerance to H 2O2, Fe2+ and Cu2+. Under these oxidant exposures, ALT301 contained lower levels of intracellular H 2O2 or lipid peroxides, and maintained higher amounts of ASA and GSH than SL. Taken together, we conclude that the accumulation of Al in cells enhances the peroxidation of lipids exclusively under growing conditions, and that the higher content of ASA and GSH in ALT301 than in SL seems to be in part responsible for the tolerance mechanism of ALT301 to Al by protecting cells from either lipid peroxidation or H2O2 commonly enhanced by Al or other oxidants.
KW - Aluminum tolerance
KW - Ascorbic acid
KW - Glutathione
KW - Oxidative stress
KW - Tobacco cells
UR - http://www.scopus.com/inward/record.url?scp=0141627964&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0141627964&partnerID=8YFLogxK
U2 - 10.1016/S0162-0134(03)00182-X
DO - 10.1016/S0162-0134(03)00182-X
M3 - Article
VL - 97
SP - 59
EP - 68
JO - Journal of Inorganic Biochemistry
JF - Journal of Inorganic Biochemistry
SN - 0162-0134
IS - 1
ER -