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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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