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Plants acquire potassium (K) not only from exchangeable K fractions but also from non-exchangeable K fractions. However, factors affecting the amount of K supplied from the non-exchangeable K fraction have not been well understood. In this study, the effects of soils and exchangeable K on the amount of K supplied to rice from the non-exchangeable K fraction were investigated for six Japanese paddy soils diluted with different rates of quartz sand. The amounts of K supplied from the non-exchangeable K fractions (recharged K) ranged from 14.4 to 137 mg K2O kg−1, equivalent to 10 to 61% of the total K acquired by rice. The amounts of recharged K were affected by the exchangeable K levels in three out of six soils. Although the cultivation experiments were conducted under various K conditions including severe K deficiency, exchangeable K was detected after cultivation in all soils, and the contents of exchangeable K were almost identical for each soil regardless of the dilution ratio of soil with quartz sand. Accordingly, there would be at least three types of non-exchangeable K fractions which dissolve into soil solution to attain a specific level of exchangeable K: (i) a non-exchangeable K fraction that releases K regardless of the exchangeable K level; (ii) a non-exchangeable K fraction that easily releases K with the decrease in exchangeable K under sufficient K conditions without inducing K-deficient symptoms in rice; and (iii) a non-exchangeable K fraction that releases K with the decrease in exchangeable K only under severe K-deficient conditions with accompanying deficient symptoms in rice. The application of K fertilizer would reduce the amount of recharged K acquired by rice from fractions (ii) and (iii), whereas fraction (i) would remain unaffected by the fertilized K until the level of exchangeable K reaches a specific level for each soil. The release of K from a fraction (iii) only occurred under conditions of severe K deficiency; hence, farmers should not rely on this fraction for K supply. [ABSTRACT FROM AUTHOR]

It has been suggested that thiol compounds such as glutathione (GSH) and phytochelatin (PC) contribute to arsenic (As) tolerance mechanisms in higher plant. In contrast, the role of thiol compounds in As tolerance and hyperaccumulation in Pteris vittata, an As hyperaccumulator fern, has not been well demonstrated so far. The purpose of this study was to elucidate that role. Gel-filtration chromatography showed that fronds of P. vittata contained high-molecular-weight As compounds containing thiol compounds. Localization of As showed similar trends to that of thiol compounds, increasing with getting higher in position of pinna. Besides, the molar ratio of thiol to As was nearly equal to the ideal molar ratio of As-thiol complexes. These results suggest that As makes complex with thiol compounds in fronds of P. vittata. When comparing P. vittata with Nephrolepis exaltata, an As nonaccumulator fern, As-induced enhancement of thiol synthesis was observed only in P. vittata. The enhancement of thiol synthesis was induced directly by As, not indirectly by As-mediated oxidative stress. γ-glutamylcysteine (γEC) synthetase is a key enzyme for the synthesis of GSH and PC. Two putative genes of γEC synthetase, PvECS1 and PvECS2, were found in P. vittata. Expression of PvECS2 in shoots increased at 48 h after the onset of As exposure, almost corresponding to the increase in concentrations of γEC and GSH. Moreover, As accumulation in shoots began just before these increases. Thus, this study strongly suggests the contribution of thiol compounds to As tolerance in P. vittata.

Rice bran contains appreciable amount of phosphorus (P), which can be used as P fertilizers. The efficiency of the P in the rice bran to plants, however, is low, and the fermentation of the rice bran is proposed to improve the P availability for plants. In the present study, 20 kg of rice bran was aerobically fermented by adding 5 kg of rice husk, 0.025 kg of mulch, and 7 L of water and incubating for 35 days with 6 times of stirring, and the changes in the chemical form of P during the fermentation process were investigated by 31P nuclear magnetic resonance spectroscopy and chemical extraction. Most part (84%) of P in the raw rice bran was myo-inositol-1,2,3,4,5,6-hexaphosphate (I6P), which is not available for plants. During the fermentation process, I6P was degraded and transformed into plant-available phosphate anions (orthophosphate). The proportions of the orthophosphate increased to 68% after incubating for 19 days with two times of stirring and 92% after incubating for 35 days with six times of stirring. After the fermentation, the orthophosphate was present as plant available precipitates associated with magnesium and the other monovalent cations. In conclusion, rice bran contains low-available I6P as a major P form, and the fermentation of rice bran accelerates the cleavage of the ester bond of I6P and results in the increased proportion of orthophosphate with high availability to plants. [ABSTRACT FROM AUTHOR]

Rhodotorula glutinis IFO1125 was found to acquire increased aluminium (AI) resistance from 50 [micro]M to more than 5 mM by repetitive culturing with stepwise increases in AI concentration at pH 4.0. To investigate the mechanism underlying this novel phenomenon, wild-type and AI-resistant cells were compared. Neither cell type accumulated the free form of AI ([AI.sup.3+]) added to the medium. Transmission electron microscopic analyses revealed a greater number of mitochondria in resistant cells. The formation of small mitochondria with simplified cristae structures was observed in the wild-type strain grown in the presence of AI and in resistant cells grown in the absence of AI. Addition of AI to cells resulted in high mitochondrial membrane potential and concomitant generation of reactive oxygen species (ROS). Exposure to AI also resulted in elevated levels of oxidized proteins and oxidized lipids. Addition of the antioxidants [alpha]-tocopherol and ascorbic acid alleviated the AI toxicity, suggesting that ROS generation is the main cause of AI toxicity. Differential display analysis indicated upregulation of mitochondrial genes in the resistant cells. Resistant cells were found to have 2.5- to 3-fold more mitochondrial DNA (mtDNA) than the wild-type strain. Analysis of tricarboxylic acid cycle and respiratory-chain enzyme activities in wild-type and resistant cells revealed significantly reduced cytochrome c oxidase activity and resultant high ROS production in the latter cells. Taken together, these data suggest that the adaptive increased resistance to AI stress in resistant cells resulted from an increased number of mitochondria and increased mtDNA content, as a compensatory response to reduced respiratory activity caused by a deficiency in complex IV function.