title: Aluminum toxicity is associated with mitochondrial dysfunction and the production of reactive oxygen species in plant cells.
abstract: Potential mechanisms of Al toxicity measured as Al-induced inhibition of growth in cultured tobacco cells (Nicotiana tabacum, nonchlorophyllic cell line SL) and pea (Pisum sativum) roots were investigated. Compared with the control treatment without Al, the accumulation of Al in tobacco cells caused instantaneously the repression of mitochondrial activities [monitored by the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and the uptake of Rhodamine 123] and, after a lag of about 12 h, triggered reactive oxygen species (ROS) production, respiration inhibition, ATP depletion, and the loss of growth capability almost simultaneously. The presence of an antioxidant, butylated hydroxyanisol, during Al treatment of SL cells prevented not only ROS production but also ATP depletion and the loss of growth capability, suggesting that the Al-triggered ROS production seems to be a cause of ATP depletion and the loss of growth capability. Furthermore, these three late events were similarly repressed in an Al-tolerant cell line (ALT301) isolated from SL cells, suggesting that the acquisition of antioxidant functions mimicking butylated hydroxyanisol can be a mechanism of Al tolerance. In the pea root, Al also triggered ROS production, respiration inhibition, and ATP depletion, which were all correlated with inhibition of root elongation. Taken together, we conclude that Al affects mitochondrial functions, which leads to ROS production, probably the key critical event in Al inhibition of cell growth.
authors.affiliation: Research Institute for Bioresources, Okayama University, Kurashiki 710-0046, Japan. yoko@rib.okayama-u.ac.jp
authors.forename: Yoko
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: S Rama
authors.initials: SR
authors.lastname: Devi
authors.forename: Sanae
authors.initials: S
authors.lastname: Rikiishi
authors.forename: Hideaki
authors.initials: H
authors.lastname: Matsumoto
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000535:Aluminum / Q000633:toxicity*; D000975:Antioxidants / Q000494:pharmacology; D002083:Butylated Hydroxyanisole / Q000494:pharmacology; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D018532:Pisum sativum / Q000166:cytology / Q000254:growth & development; D059828:Plant Cells; D063245:Plant Development; D018517:Plant Roots / Q000166:cytology / Q000254:growth & development; D017382:Reactive Oxygen Species / Q000378:metabolism*; D020112:Rhodamine 123 / Q000378:metabolism; D013778:Tetrazolium Salts / Q000378:metabolism; D013844:Thiazoles / Q000378:metabolism; D014026:Nicotiana / Q000166:cytology / Q000254:growth & development
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D013778:Tetrazolium Salts; D013844:Thiazoles; D020112:Rhodamine 123; D002083:Butylated Hydroxyanisole; D000255:Adenosine Triphosphate; D000535:Aluminum; C022616:thiazolyl blue