PubMed Health⌕ Search

PubMed · 9684403

Kalman filtering-aided time-resolved solid-surface room temperature phosphorimetry for simultaneous determination of anthracyclines in solution.

Abstract

Daunorubicin, doxorubicin and epirubicin react with EuIII to form complexes which exhibit analytically useful room temperature phosphorescence (RTP). The RTP features of the three complexes are similar and the RTP spectra completely overlap. However, their three phosphorescence decay rates are different, and these differences were utilized to analyse the time-resolved RTP data by Kalman filtering. Simultaneous quantification of all three complexes is demonstrated and a method is proposed for the simultaneous determination of the three anthracyclines in mixtures by RTP optosensing. The analytical errors observed are within +/- 5%.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

F Alava-Moreno, M J Valencia-González, M E Díaz-García. 1998. Kalman filtering-aided time-resolved solid-surface room temperature phosphorimetry for simultaneous determination of anthracyclines in solution.. https://doi.org/10.1039/a704795i

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Tropomyosin-1, a novel suppressor of cellular transformation is downregulated by promoter methylation in cancer cells.

Tropomyosins (TMs) are a family of microfilament binding proteins, which are suppressed in the transformed cells. We have investigated the mechanism of suppression of TMs, in particular that of tropomyosin-1 (TM1), in breast cancer cells. Inhibition of DNA methyl transferase with 5-aza-2'-deoxycytidine (AZA) alone did not induce TM1 expression. However, combined treatment of trichostatin A (TSA) and AZA resulted in readily detectable expression of TM1, but not that of other TM isoforms. Upregulation of TM1 expression paralleled with the reemergence of TM1 containing microfilaments, and in abolition of anchorage-independent growth. The synergistic action of AZA and TSA in reactivation of TM1 gene was also evident in ras-transformed fibroblasts. These data, for the first time, show that hypermethylation of TM1 gene and chromatin remodeling are the predominant mechanisms by which TM1 expression is downregulated in breast cancer cells.

Antibiotics, Antineoplastic↗

Neocarzinostatin induces Mre11 phosphorylation and focus formation through an ATM- and NBS1-dependent mechanism.

DNA double-strand breaks, if unrepaired, may lead to the accumulation of chromosomal aberrations and eventually cancer cell formation. Components of the Rad50/NBS/Mre11 nuclease complex are essential for the effective repair of DNA double-stranded breaks. Here, we show that neocarzinostatin, a radiomimetic enediyne antibiotic, induces phosphorylation and nuclear focus formation of Mre11 and NBS1 through a cell cycle-independent mechanism. Furthermore, neocarzinostatin-induced Mre11 phosphorylation and nuclear focus formation are defective in AT and NBS cells, but not wild type cells. Our results suggest that ATM and NBS1 are required for the effective repair of neocarzinostatin-induced DNA double-strand breaks by both non-homologous end joining and homologous recombinational repair pathways.

Antibiotics, Antineoplastic↗

Total synthesis of deamido bleomycin a(2), the major catabolite of the antitumor agent bleomycin.

Metabolic inactivation of the antitumor antibiotic bleomycin is believed to be mediated exclusively via the action of bleomycin hydrolase, a cysteine proteinase that is widely distributed in nature. While the spectrum of antitumor activity exhibited by the bleomycins is believed to reflect the anatomical distribution of bleomycin hydrolase within the host, little has been done to characterize the product of the putative inactivation at a chemical or biochemical level. The present report describes the synthesis of deamidobleomycin demethyl A(2) (3) and deamido bleomycin A(2) (4), as well as the respective aglycones. These compounds were all accessible via the key intermediate N(alpha)-Boc-N(beta)-[1-amino-3(S)-(4-amino-6-carboxy-5-methylpyrimidin-2-yl)propion-3-yl]-(S)-beta-aminoalanine tert-butyl ester (16). Synthetic deamido bleomycin A(2) was shown to be identical to the product formed by treatment of bleomycin A(2) with human bleomycin hydrolase, as judged by reversed-phase HPLC analysis and (1)H NMR spectroscopy. Deamido bleomycin A(2) was found to retain significant DNA cleavage activity in DNA plasmid relaxation assays and had the same sequence selectivity of DNA cleavage as bleomycin A(2). The most significant alteration of function noted in this study was a reduction in the ability of deamido bleomycin A(2) to mediate double-strand DNA cleavage, relative to that produced by BLM A(2).

Antibiotics, Antineoplastic↗