Effects of aluminum in red spruce (Picea rubens) cell cultures: Cell growth and viability, mitochondrial activity, ultrastructure and potential sites of intracellular aluminum accumulation
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Physiologia Plantarum. 113: 486-498.
The effects of Al on red spruce (Picea rubens Sarg.) cell suspension cultures were examined using biochemical, stereo-logical and microscopic methods. Exposure to Al for 24-48 h resulted in a loss of cell viability, inhibition of growth and a significant decrease in mitochondrial activity. Soluble protein content increased in cells treated with Al. Using energy-dispersive X-ray microanalysis on sections of freeze-substituted cells that had no obvious disruption in cytoplasmic or cell wall structure, Al (always in the presence of P) was detected in dense regions in cell walls, cytoplasm, plastids and vacuoles after 48 h exposure to Al. Stereological quantification of spruce cell structure showed that, after 24 h of Al treatment, intact cells had increased vacuolar and total cell volume, but the nuclear volume did not change. In addition, Al treatment resulted in increased surface area of Golgi membranes and endoplasmic reticulum. The biochemical and ultrastructural alterations in red spruce cells, in combination with the presence of Al in cellular organelles of visually intact cells, suggest that Al movement occurred across the plasma membrane without major cellular disruption. Detailed short-term time course studies are needed to determine if intracellular Al in these cells results from its passage into cells through sub-microscopic lesions in the plasma membrane or it is taken up into the symplast through the intact membrane by an active, but slow, process.
Minocha, Rakesh; McQuattie, Carolyn; Fagerberg, Wayne; Long, Stephanie; Noh, Eun Woon. 2001. Effects of aluminum in red spruce (Picea rubens) cell cultures: Cell growth and viability, mitochondrial activity, ultrastructure and potential sites of intracellular aluminum accumulation. Physiologia Plantarum. 113: 486-498. https://doi.org/10.1034/j.1399-3054.2001.1130407.x.