Effects of aluminum toxicity on nutrient accumulation in maize shoots: Implications on photosynthesis

Abstract

The physiological characterization of aluminum (Al) toxicity in C4 plants prompted this study, having maize (Zea mays cv. XL‐72.3) used as a test system. Two weeks after germination, maize plants were submitted to increasing Al concentrations (from 0 up to 81 mg L‐1) for 20 days in a growth medium with low ionic strength, after which several analyses were carried out. In root tissues, Al concentrations significantly increased between the 0 and the 81 mg L‐1 Al treatment. In the shoots nitrogen (N), phosphorus (P), and iron (Fe) significantly decreased with increasing Al concentrations, but at different rates. Magnesium (Mg) showed a tendency to decrease for Al treatments higher than 9 mg L‐1, the opposite occurring with manganese (Mn) contents. Chlorophyll a fluorescence parameters Fo and Fv/Fm showed non‐significant changes, while photosynthetic capacity, electron transport rate associated with photosystem I and cytochromes (cyt) f and b563 contents decreased above the 9 mg L‐1 Al treatment. Aluminum concentrations were correlated to phenol and quinone contents. In isolated chloroplasts, acyl lipid peroxidation increased continuously until the 81 mg L‐1 Al treatment, whereas ethylene production in intact leaves showed a sharp rise already for the 9 mg L‐1 Al treatment. Increasing Al concentrations significantly inhibited copper (Cu), zinc (Zn)‐SOD, catalase and glutathione reductase activities, whereas those of ascorbate peroxidase and dehydroascorbate reductase increased, in Al treatments with 9 mg L‐1 or higher. It was concluded that Al toxic effects in the shoot metabolism were mostly indirect, being mediated/modulated by the interactions between root Al concentrations and the concurrent inhibition of nutrients translocation mechanism(s). It was further concluded that an increasing production of chloroplastic hydroxyl radicals is coupled to the initial targets of Al mediated/modulated toxicity, being the intrachloroplastic production of H2O2, superoxide and singlet oxygen limited. It was also found, a decreased efficiency on the control of superoxide and H2O2 accumulation, since Cu,Zn‐SOD activity was ihibited and because the in vivo ascorbate peroxidase activity was limited by that of glutathione reductase. Additionally, as catalase activity was inhibited, the control of the concentration of photosynthetically‐generated H2O2 that might diffuse out of the chloroplast was also found to be less effective.