Effect of salicylic acid on the attenuation of aluminum toxicity in Coffea arabica L. suspension cells: A possible protein phosphorylation signaling pathway

• Growth inhibition produced by aluminum is restored by treatment with Al and SA.
• The inhibition of phospholipase C by the Al treatment was restored during the exposure to SA and Al.
• SA attenuation of aluminum toxicity could be linked to protein phosphorylation.

The protective effect of salicylic acid (SA) on aluminum (Al) toxicity was studied in suspension cells of Coffea arabica L. The results showed that SA does not produce any effect on cell growth and that the growth inhibition produced by aluminum is restored during simultaneous treatment of the cells with Al and SA. In addition, the cells exposed to both compounds, Al and SA, showed evident morphological signals of recovery from the toxic state produced in the presence of Al. The cells treated with SA showed a lower accumulation of Al, which was linked to restoration from Al toxicity because the concentration of Al3 + outside the cells, measured as the Al3 +–morin complex, was not modified by the presence of SA. Additionally, the inhibition of phospholipase C by Al treatment was restored during the exposure of the cells to SA and Al. The involvement of protein phosphorylation in the protective effect of SA on Al-toxicity was suggested because staurosporine, a protein kinase inhibitor, reverted the stimulatory effect of the combination of Al and SA on protein kinase activity. These results suggest that SA attenuates aluminum toxicity by affecting a signaling pathway linked to protein phosphorylation.

The growth inhibition that is produced by aluminum is restored by salicylic acid. The inhibition of phospholipase C by the Al was restored in the presence of SA. These results suggested that SA attenuated aluminum toxicity likely by affecting a signaling pathway linked to protein phosphorylation.Figure optionsDownload as PowerPoint slide