The time-concentration interaction of Al toxicity in wheat root meristems Public Deposited

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  • The time-concentration interaction of Al toxicity in the root meristems of Brevor wheat was studied using the L.D. 50 as a criteria for Al damage. The L.D. 50 represented a precise, well defined degree of biological damage which was easily reproduced under conditions where factors like temperature, pH, nutrient concentration, Al concentration, and time of exposure were rigidly controlled. A diffusion-absorption model was developed to explain the time-concentration interaction of Al toxicity in wheat root meristems. The model attributed the L.D. 50 to the accumulation within meristematic cells of a fixed quantity of Al. The model predicted that above a certain time, the t(L.D. 50)- reciprocal concentration relationship should be linear with the data extrapolating to positive intercepts on the time axis. Wheat roots of the variety, Brevor, were found to yield data that when plotted as t(L.D. 50) versus reciprocal concentration were linear for Al concentrations as high as 50 ppm and did have positive intercepts on the time axis. A linear relationship was obtained regardless of the salt concentration or the pH. It was observed that lateral roots were much more sensitive to Al than primary roots at all concentrations used in this study. The t(L.D. 50)- reciprocal concentration relationship for lateral roots not only had a smaller slope than that for primary roots, but also extrapolated to smaller intercepts on the time axis. This behavior was shown to be in agreement with the predictions of the model where meristematic size was the only variable. The model suggested that the effect of salt concentration on Al toxicity in Brevor wheat is on the uptake of Al by meristematic cells. The model could not account for the salt effect by changes in the diffusion coefficient or the complexing of Al by cell walls or other material outside the cell. The model further suggested that the Al uptake rate is "hyperbolic" with concentration. This would be in agreement with what is known about the uptake of many other solutes, both organic and inorganic as well. The pH was found to have two effects on the toxicity of Al. One was an effect during pretreatment prior to Al exposure. Increasing the pH at which the seeds were germinated from 4 to 5 resulted in a small but consistent increase in the t(L.D. 50) obtained during a subsequent Al exposure. The mechanism by which pretreatment pH affects the subsequent toxicity of Al was speculated to be a detrimental effect of H+ on the membranes during their development. The other effect of pH was observed during the Al treatment. Increasing the pH of an Al solution from 4.0 to 4.5 increased the toxicity of Al. The effect of pH on the t(L.D.50)-reciprocal concentration relationship was to lower the slope but have no effect on the extrapolated intercept. The increase in toxicity was shown to be too small to be accounted for by increases in the concentration of AlOH⁺² or Al(OH)⁺¹ ₂ calculated from known thermodynamic equilibrium constants. In addition, increasing the pH from 4. 5 to 4.7 did not further increase the toxicity of Al. This lack of response of Al toxicity between pH 4.5 and 4.7 was apparently not the result of precipitation of Al under these experimental conditions. The evidence suggested that there may be other processes in addition to hydrolysis which affect the toxicity of Al as the pH is raised. Experiments using the metabolic inhibitor, DNP, during an Al treatment suggested that Al uptake by meristematic cells is probably the result of passive diffusion across the plasmalemma. Under these conditions, the permeability of cell membranes would be a controlling factor in the rate of Al uptake. A mechanism was proposed in which the increased toxicity of Al with pH was attributed to both the hydrolysis of Al and the known effects of pH on membrane permeability.
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