Journal
PLANT AND SOIL
Volume 363, Issue 1-2, Pages 399-410Publisher
SPRINGER
DOI: 10.1007/s11104-012-1396-z
Keywords
Aluminum; Oxidative stress; Pea root; Programmed cell death; Recovery; Toxicity
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Funding
- Japanese Ministry of Education, Sports, Science and Technology [2258007]
- Grants-in-Aid for Scientific Research [22580072] Funding Source: KAKEN
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Although many studies on the mechanism of Al toxicity and tolerance have been conducted independently, events occurring during the recovery process from Al injury is limited. This study was to investigate Al toxicity recovery mechanism focusing in morphological and physiological aspect. We investigated the mechanisms underlying Al toxicity recovery in terms of oxidative stress using the pea root apex as a model system. The accumulation of reactive oxygen species was remarkably high in the root under continued Al treatment but decreased in the recovering root. The superoxide anion exuded in the presence of nicotinamide adenine dinucleotide phosphate (NADPH) showed a similar tendency with respect to the accumulation of reactive oxygen species. A similar pattern of lignin content and superoxide dismutase activity was observed among the treatments, while the increased peroxidation in the root under continued Al treatment did not decline with recovery treatment. A longitudinal section of the root under continued Al treatment showed the accumulation of superoxide anion, lignin and peroxide (H2O2) at the epidermal and outer cortex region where the Al induced injuries, including ruptures, are detected. Oxidative stress is associated with the mechanism of Al toxicity recovery. The recovery process might include the elongation of the central cylinder as a consequence of the oxidative stress-induced formation of the zonal region (ZR). The results further suggest a plausible role for the ZR in the programmed cell death-like function involved in Al toxicity recovery.
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