Phenylpropanoids as a Protectant of Aluminum Toxicity in Cultured Tobacco Cells

Abstract

Aluminum (Al) enhances ferrous ion [Fe(II)]-mediated peroxidation of lipids, which is lethal to normal tobacco cells, but not to phosphate (Pi)-starved cells ( −P cells). We found that tobacco cells accumulated phenylpropanoid compounds including chlorogenic acid (CGA) and caffeic acid (CA) during Pi 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 Pi 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)