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Plant Physiol, January 2002, Vol. 128, pp. 63-72

Aluminum Toxicity Is Associated with Mitochondrial Dysfunction and the Production of Reactive Oxygen Species in Plant Cells1

Yoko Yamamoto,* Yukiko Kobayashi, S. Rama Devi, Sanae Rikiishi, and Hideaki Matsumoto

Research Institute for Bioresources, Okayama University, Kurashiki 710-0046, Japan (Y.Y., Y.K., S.R.D., S.R., H.M.); and Bio-Oriented Technology Research Advancement Institution, 1-40-2 Nisshin-cho, Omiya 331-8537, Japan (S.R.D.)

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.

1 This work was supported by the Program for Promotion of Basic Research Activities for Innovative Biosciences (to H.M.), by the Ministry of Education, Culture, Sports, Science and Technology of Japan (Grant-in-Aid for General Scientific Research no. 11306006 to H.M.), and by the Ohara Foundation for Agricultural Science.

* Corresponding author; e-mail yoko{at}rib.okayama-u.ac.jp; fax 81-86-434-1210.

© 2002 American Society of Plant Physiologists


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