PubMed HealthSearch

PubMed · 6109566

Failure of aclacinomycin and 7-con-O-methylnogarol (7-OMEN) to decrease cardiac guanylate cyclase activity.

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B A Levey, E Ruiz, B Rogerson, D C Lehotay, G S Levey. Failure of aclacinomycin and 7-con-O-methylnogarol (7-OMEN) to decrease cardiac guanylate cyclase activity.. https://pubmed.ncbi.nlm.nih.gov/6109566/

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

KEEP EXPLORING

Related citations

Inhibition of different steps of the ubiquitin system by cisplatin and aclarubicin.

Ubiquitin is involved in such fundamental cellular processes as cell cycle control, DNA repair, protein degradation and stress responses. We previously reported that cisplatin could inhibit the ubiquitin-ATP-dependent proteolysis and ubiquitination. We further investigated the effect of various antitumor agents on the ubiquitin system and found that aclarubicin (ACR) inhibits the ubiquitin-ATP-dependent proteolysis but not the ubiquitination process. We found that ACR as well as cisplatin inhibited the ubiquitin-ATP-dependent proteolytic activity of rabbit reticulocytes. The IC50 values of these agents were 52 and 90 microM, respectively. Although cisplatin inhibits the conjugation of ubiquitin to proteins through the inhibition of a ubiquitin-activating enzyme, ACR, at 120 microM, does not. Thus, the antitumor agents affecting the ubiquitin system could be classified into two groups; one is represented by cisplatin, which inhibits the ubiquitination of the proteins, and the other is ACR, which does not inhibit the ubiquitination but does inhibit the ubiquitin-ATP-dependent proteolysis. Mitomycin C belongs to the latter group.

Aclarubicin

Thermodynamics of the anthracycline-nuclei interactions in drug-resistant and drug-sensitive K562 cells.

Fluorescence emission spectra from anthracycline-treated cells suspended in buffer have been used to measure the uptake of three anthracycline derivatives: Adriamycin (ADR), 4'-o-tetrahydropyranyl-Adriamycin (THP-ADR) and aclacinomycin (ACM) in drug-sensitive and drug-resistant K562 cells. The concentration of drug bound to the nucleus and free in the cytoplasm, at steady state, as well as the concentration of drug bound to the nucleus at equilibrium state have been determined at temperatures ranging from 6 degrees to 40 degrees. The enthalpies for the binding of ADR, THP-ADR and ACM to nuclei equal -35 +/- 3, -35 +/- 3 and -30 +/- 3 kJ/mol, respectively. These values compare with the enthalpies of binding of these drugs to naked DNA.

Aclarubicin

Kinetic parameters for the uptake of anthracycline by drug-resistant and drug-sensitive K562 cells.

Fluorescence-emission spectra from anthracycline-treated cells suspended in buffer have been used to measure the uptake of three anthracycline derivatives: adriamycin, 4'-O-tetrahydropyranyladriamycin and aclacinomycin in drug-sensitive and drug-resistant K562 cells. The initial rate of uptake and the kinetics of active efflux under the effect of an integral membrane glycoprotein, P-glycoprotein, have been measured as a function of temperature. The activation energies for the passage of the drugs through the plasma membrane have been calculated. In the case of 4'-O-tetrahydropyranyladriamycin, the activation energies for the passive diffusion of the drug equal 45 kJ.mol-1 and 37 kJ.mol-1 for sensitive and resistant cells, respectively. The activation energy for the active efflux of 4'-O-tetrahydropyranyladriamycin equal 25 kJ.mol-1.

Aclarubicin