Search results for: Amintra NiHIS _ 100 ml
#26162706 2015/06/19 To Up
Root uptake and translocation of nickel in wheat as affected by histidine.
The role of histidine (His) on root uptake, xylem loading and root to shoot transport of nickel (Ni) was investigated in a winter (Triticum aestivum cv. Back Cross) and a durum wheat (Triticum durum cv. Durum) cultivar. Seedlings were grown in a modified Johnson nutrient solution and exposed to 10 μM of Ni and 100 μM of histidine (His) as no His, Ni (10) + His (100) and Ni(His) in a 1:1 mole ratio (1:1) complex. In our study, the presence of vanadate (a metabolic inhibitor) resulted in a significant decrease of root Ni uptake, indicating that a part of Ni uptake by the plant root is energy-dependent. Addition of His significantly increased the Ni content in shoots and roots of both wheat cultivars. The data suggest that the Ni(His) is most likely to be taken up as a complex or receptors at the membrane are able to enhance Ni uptake from Ni(His) complex. This result was indirectly supported by using EDTA as a strong chelating reagent to reduce the uptake of Ni(His) complexes. By using this ligand, the xylem loading of Ni and His was disproportionately reduced. Cycloheximide (a translation inhibitor) strongly decreased the release of His and Ni from the root into the xylem of wheat, suggesting the significance of a symplastic pathway for Ni loading into the xylem.Neda Dalir, Amir Hossein Khoshgoftarmanesh
2814 related Products with: Root uptake and translocation of nickel in wheat as affected by histidine.
24 tests100 μg100 assays100 μg20 96 samples1 kit100 assays96 assays 96 samples400TestsRelated Pathways
#3093908 // To Up
Copper stimulation of LHRH release from median eminence explants. I. A divalent metal specific process that does not require extracellular calcium.
We have previously shown that chelated copper stimulates the release of LHRH from explants of the median eminence area (MEA) incubated under in vitro conditions, and that this stimulation involves a ligand specific interaction. To further elucidate the mechanism of action of copper, we addressed two questions: (a) What is the divalent metal [metal(II)] specificity for this release process? (b) Is the stimulation of LHRH release by CuHis dependent on influx of extracellular calcium? MEA obtained from adult male rats were incubated for 15 min with one of the following divalent metals Cu, Ni, Fe, Zn, Cd or Mn (each complexed to histidine at an equimolar ratio; 100 microM) and then in the absence of metal for an additional period of 30 min. We found that CuHis and to a lesser extent NiHis stimulated LHRH release, and that FeHis, ZnHis, CdHis or MnHis did not do so. In addition, MEA were incubated for 15 min with CuHis in the presence or absence of CaCl2. Under these two conditions, the temporal pattern and magnitude of CuHis-stimulated LHRH release were identical, indicating that extracellular calcium is not required for copper action. Since, in this series of metals, Cu2+ and Ni2+ are the most potent oxidizing agents, our finding strongly supports our previous proposition that an oxidation reaction is involved in the process of copper stimulation of LHRH release. It has yet to be elucidated whether copper action is totally independent of an increase in intracellular calcium or whether copper leads to LHRH release via mobilization of calcium from intracellular stores.M Colombani-Vidal, A Barnea
1849 related Products with: Copper stimulation of LHRH release from median eminence explants. I. A divalent metal specific process that does not require extracellular calcium.
100ug100μg500 rxns4 Membranes/Box250 assays0.2 mg2 Pieces/Box100ug Lyophilized100μg100 Plates100ug Lyophilized100ugRelated Pathways
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