PubMed · 6696484
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T M Kelly, L M Fishman, H E Lessner. 1984. Hyperpigmentation with daunorubicin therapy.. https://pubmed.ncbi.nlm.nih.gov/6696484/
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A novel COOH+ ion implantation-modified indium tin oxide (COOH/ITO) electrode was prepared for the first time and applied for determination of daunomycin (or daunorubicin [DNR]). The electrode showed higher catalytic activity than bare ITO electrode with good reproducibility and stability. The determination condition of linear voltammetry was optimized. A calibration curve was obtained over the range 2.0 x 10(-7) to 5.0 x 10(-6)mol/L, with a correlation coefficient of 0.9909 and a limit of detection of 1.0 x 10(-7)mol/L. The selectivity of the electrode was illustrated by determination of DNR in samples prepared of urine. X-ray photoelectron spectroscopy (XPS) analysis results showed that the implanted COOH+ maintained characteristics of organic group -COOH. A field emission-scanning electron microscope (FSEM) result showed that the implanted surface caused defects and partial dislocations and formed many active centers.
WP631, a new DNA-binding drug that bisintercalates into DNA with high affinity, seems to be highly cytotoxic against Jurkat T lymphocytes. The purpose of this study was to gain new insights into the mechanisms by which WP631 halts proliferation in this cell type. Treating Jurkat cells with nanomolar concentrations of WP631 produced G(2)/M arrest, inhibited the transcription of c-myc and p53 genes, and induced limited apoptosis during the duration of treatment. Suppression of c-myc and p53 expression, and time-dependent decline in c-Myc and p53 protein levels, was associated with growth arrest. A weak interdependence was also found between the potent antiproliferative activity and the apoptotic response; treatment with WP631 for 24-36hr produced arrest in G(2)/M and allowed for partial DNA repair. Longer treatments with WP631 allowed some repaired cells to re-enter the cell cycle, but produced aneuploidy or apoptosis in others.
The stability of cellular membranes during dehydration can be strongly influenced by the partitioning of amphiphilic solutes from the aqueous phase into the membranes. The effects of partitioning on membrane stability depend in a complex manner on the structural properties of the amphiphiles and on membrane lipid composition. Here, we have investigated the effects of the amphiphilic aromatic amino acids Trp and Phe on membrane stability during freezing. Both amino acids were cryotoxic to isolated chloroplast thylakoid membranes and to large unilamellar liposomes, but Trp had a much stronger effect than Phe. In liposomes, both amino acids induced solute leakage and membrane fusion during freezing. The presence of the chloroplast galactolipids monogalactosyldiacylglycerol or digalactosyldiacylglycerol in egg phosphatidylcholine (EPC) membranes reduced leakage from liposomes during freezing in the presence of up to 5 mM Trp, as compared to membranes composed of pure EPC. The presence of the nonbilayer-forming lipid phosphatidylethanolamine increased leakage. Membrane fusion followed a similar trend, but was dramatically reduced when the anthracycline antibiotic daunomycin was incorporated into the membranes. Daunomycin has been shown to stabilize the bilayer phase of membranes in the presence of nonbilayer lipids and was therefore expected to reduce fusion. Surprisingly, this had only a small influence on leakage. Collectively, these data indicate that Trp and Phe induce solute leakage from liposomes during freezing by a mechanism that is largely independent of fusion events.