ArticlePlant physiology2010
The involvement of lipid peroxide-derived aldehydes in aluminum toxicity of tobacco roots.
Article in Plant physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 151 citations in OpenAlex.
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- Transcriptomic responses to aluminum stress in tea plant leaves.Scientific reports · 2021Article
- New sources of lentil germplasm for aluminium toxicity tolerance identified by high throughput hydroponic screening.Physiology and molecular biology of plants : an international journal of functional plant biology · 2021Article
- Lipid Peroxide-Derived Reactive Carbonyl Species as Mediators of Oxidative Stress and Signaling.Frontiers in plant science · 2021Review
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- A Role for Tocopherol Biosynthesis in Arabidopsis Basal Immunity to Bacterial Infection.Plant physiology · 2019Article
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- A concise appraisal of lipid oxidation and lipoxidation in higher plants.Redox biology · 2019Review
- Extracellular silica nanocoat formed by layer-by-layer (LBL) self-assembly confers aluminum resistance in root border cells of pea (Pisum sativum).Journal of nanobiotechnology · 2019Article
- Phosphorus-mediated alleviation of aluminum toxicity revealed by the iTRAQ technique in Citrus grandis roots.PloS one · 2019Article
- Detoxification of Reactive Carbonyl Species by Glutathione Transferase Tau Isozymes.Frontiers in plant science · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative injury of the root elongation zone is a primary event in aluminum (Al) toxicity in plants, but the injuring species remain unidentified. We verified the hypothesis that lipid peroxide-derived aldehydes, especially highly electrophilic alpha,beta-unsaturated aldehydes (2-alkenals), participate in Al toxicity. Transgenic tobacco (Nicotiana tabacum) overexpressing Arabidopsis (Arabidopsis thaliana) 2-alkenal reductase (AER-OE plants), wild-type SR1, and an empty vector-transformed control line (SR-Vec) were exposed to AlCl(3) on their roots. Compared with the two controls, AER-OE plants suffered less retardation of root elongation under AlCl(3) treatment and showed more rapid regrowth of roots upon Al removal. Under AlCl(3) treatment, the roots of AER-OE plants accumulated Al and H(2)O(2) to the same levels as did the sensitive controls, while they accumulated lower levels of aldehydes and suffered less cell death than SR1 and SR-Vec roots. In SR1 roots, AlCl(3) treatment markedly increased the contents of the highly reactive 2-alkenals acrolein, 4-hydroxy-(E)-2-hexenal, and 4-hydroxy-(E)-2-nonenal and other aldehydes such as malondialdehyde and formaldehyde. In AER-OE roots, accumulation of these aldehydes was significantly less. Growth of the roots exposed to 4-hydroxy-(E)-2-nonenal and (E)-2-hexenal were retarded more in SR1 than in AER-OE plants. Thus, the lipid peroxide-derived aldehydes, formed downstream of reactive oxygen species, injured root cells directly. Their suppression by AER provides a new defense mechanism against Al toxicity.
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