Phenylpropanoids as a Protectant of Aluminum Toxicity in Cultured Tobacco Cells

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Aluminum(Al) enhances ferrous ion [Fe(II)]-mediated peroxidation of lipiss, 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).
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