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The application of the biostimulant tablet containing both G and T can promote transplant establishment and vegetable crop productivity in a sustainable way.

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Treatment of K562 cells, a human erythroleukemia cell line, with desferrioxamine raised the levels of the receptor for transferrin (Tf) two-to threefold over that of the control cells. The levels of receptor were reduced by at least 50 and 35% of that of the control in cells treated with diferric Tf and ferric ammonium citrate, respectively. These changes were of total cellular receptors with no alteration in the proportion of receptors found on the cell surface. The half-lives of the receptor were identical in cells treated with desferrioxamine, diferric Tf, or ferric ammonium citrate. Cells metabolically labeled with [35S]methionine showed a 2.5-fold increase in the rate of receptor synthesis when treated with desferrioxamine and a 35 and 65% decrease when treated with ferric ammonium citrate and diferric Tf, respectively. In vitro translations of. polyadenylated mRNA isolated from cells incubated with desferrioxamine showed a 2.5-fold increase in translatable mRNA for the receptor, whereas treatment of cells with ferric ammonium citrate and diferric Tf resulted in a 25 and 50% reduction, respectively, in translatable mRNA for this receptor.Iron is an essential constituent of all cells. It is required for the normal functioning of a wide array of cellular enzymes, including those of the respiratory pathway (2, 4, 6). Cells receive iron via the receptor-mediated endocytosis of irontransferrin (Tf). Large amounts of iron can be stored in cells in ferritin and as hemosiderin. The iron needs of cells vary and are high in fetal, erythropoietic, and rapidly proliferating cells. Concomitant with these needs is a high level of expression of Tf receptors in placental cells, reticulocytes, and proliferating cells (1,8,10). It is not known exactly how cells regulate their iron uptake, but clearly the modulation of the number of Tf receptors can play a role in such regulation. Recently, Bridges et al. (Fed. Proc. 42:2193 and Mattia et al. (9) showed that K562 cells can alter Tf receptor numbers in response to intracellular iron chelation by desferrioxamine. The locus of this regulation was shown to be at the level of mRNA for the receptor (9). Ward et al. (12) reported a down regulation of Tf receptors in HeLa cells that were treated with iron salts. In this paper we report the extension of our studies on the regulation of Tf receptor biosynthesis in K562 cells. We show that delivering iron to cells results in a twofold decrease in specific synthesis of the Tf receptor. A decrease in the levels of mRNA is responsible for this drop. Furthermore, we compare the efficacy of Tf with that of ferric ammonium citrate in lowering receptor biosynthesis and establish the range of receptor regulation achievable with iron depletion or iron introduction without causing observable cellular toxicity.