TY - JOUR
T1 - Phenylpropanoids as a protectant of aluminum toxicity in cultured tobacco cells
AU - Yamamoto, Yoko
AU - Hachiya, Akiko
AU - Hamada, Hiroki
AU - Matsumoto, Hideaki
N1 - Funding Information:
The authors are grateful to Dr. N. Amrhein (Institute of Plant Sciences, Swiss Federal Institute of Technology, Switzerland) for his kind gift of AIP, JASCO International Co. Ltd. for providing the MS spectra and Dr. T. Yoshida (Okayama Univ., Japan) for his useful suggestions about antioxidant effects of phenolic compounds. This work was supported in part by a Grant-in-Aid for General Scientific Research (no. 08640829) from the Ministry of Education, Science, Sports and Culture of Japan, the Ohara Foundation for Agricultural Science, Hayashi Memorial Foundation for Female Natural Scientists, and Showa Shell Sekiyu Foundation for the Promotion of Environmental Research.
PY - 1998/9
Y1 - 1998/9
N2 - Aluminum (Al) enhances ferrous ion [Fe(II)]-mediated peroxidation of lipids, which is lethal to normal tobacco cells, but not to phosphate (P(i))-starved cells (-P cells). We found that tobacco cells accumulated phenylpropanoid compounds including chlorogenic acid (CGA) and caffeic acid (CA) during P(i) starvation. The accumulation was inhibited by 2-aminoindan-2-phosphonic acid (AIP), a specific inhibitor of L-phenylalanine ammonia lyase (PAL). CGA, CA and also an extract containing the phenylpropanoid compounds from -P cells protected normal cells (+P cells) efficiently from both lipid peroxidation and the loss of viability caused by the combined application of Al and Fe(II), indicating that the phenylpropanoids acted as antioxidant molecules. -P cells exhibited approximately 25-fold higher specific activity of PAL than +P cells. The content of the phenylpropanoids and the activity of PAL were not affected by the combined treatment with Al and Fe(II) in either +P cells or -P cells. These results suggest that an increase in PAL activity during P(i) starvation enhances the accumulation of phenylpropanoids, and that the phenylpropanoids protect tobacco cells from cytotoxic lipid peroxidation caused by the combination of Al and Fe(II).
AB - Aluminum (Al) enhances ferrous ion [Fe(II)]-mediated peroxidation of lipids, which is lethal to normal tobacco cells, but not to phosphate (P(i))-starved cells (-P cells). We found that tobacco cells accumulated phenylpropanoid compounds including chlorogenic acid (CGA) and caffeic acid (CA) during P(i) starvation. The accumulation was inhibited by 2-aminoindan-2-phosphonic acid (AIP), a specific inhibitor of L-phenylalanine ammonia lyase (PAL). CGA, CA and also an extract containing the phenylpropanoid compounds from -P cells protected normal cells (+P cells) efficiently from both lipid peroxidation and the loss of viability caused by the combined application of Al and Fe(II), indicating that the phenylpropanoids acted as antioxidant molecules. -P cells exhibited approximately 25-fold higher specific activity of PAL than +P cells. The content of the phenylpropanoids and the activity of PAL were not affected by the combined treatment with Al and Fe(II) in either +P cells or -P cells. These results suggest that an increase in PAL activity during P(i) starvation enhances the accumulation of phenylpropanoids, and that the phenylpropanoids protect tobacco cells from cytotoxic lipid peroxidation caused by the combination of Al and Fe(II).
KW - Aluminum
KW - Lipid peroxidation
KW - Nicotiana tabacum
KW - Phenylalanine ammonia lyase
KW - Phenylpropanoid
KW - Phosphate starvation
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U2 - 10.1093/oxfordjournals.pcp.a029459
DO - 10.1093/oxfordjournals.pcp.a029459
M3 - Article
AN - SCOPUS:0031719848
SN - 0032-0781
VL - 39
SP - 950
EP - 957
JO - Plant and Cell Physiology
JF - Plant and Cell Physiology
IS - 9
ER -