The inhibition of growth of tobacco cells (Nicotiana tabacum L. cv. Samsun) after treatment with A1 in medium containing high concentrations of cations requires the presence of Fe (II or III) during the treatment. We examined whether the inhibition of the post‐treatment growth is due to cell death occurring during the treatment with A1 and Fe. In cells at the end of A1 treatment, the integrity of the plasma membrane and the integrity of the mitochondrial inner membrane were monitored by use of Evans blue staining and the cleavage of 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide (MTT), respectively. Time‐course and dose‐response experiments indicate that the inhibition of post‐treatment growth is strongly related to Evans blue uptake, but not to MTT cleavage. These results suggest that the loss of integrity of the plasma membrane caused by a combination of Al and Fe directly contributes to cell death and the inhibition of post‐treatment growth.

cells were prepared by culturing cells with buthionine sulfox-The role of endogenous glutathione (GSH) in the protection of suspension-cultured tobacco cells from aluminum (Al) toxicityimine (an inhibitor of -glutamylcysteine synthetase) for 24 h. was examined. Cells at the logarithmic phase of growth were Total GSH content in GSH-deprived cells was 6% of that in normal cells. The GSH-deprived cells exhibited a higher treated with or without Al in nutrient medium prepared withdegree of lipid peroxidation, increased accumulation of Al, out P i and EDTA. In the absence of Al, total GSH content and greater loss of viability than normal cells. These results (including oxidized glutathione [GSSG]) increased gradually.suggest that GSH protects cells from the oxidative membrane In the presence of Al, the increase of GSH was repressed. damage caused by a combination of Al and Fe(II) possibly by This effect was observed before the loss of plasma membrane integrity and the loss of cell viability. In contrast, GSSG both direct consumption of GSH and oxidation of GSH. content in cells increased in the presence of Al. GSH-deprived

No abstract