Casiopeínas® are copper complexes with the general formula [Cu(N-N)(N-O)]NO(3) and [Cu(N-N)(O-O)]NO(3) where N-N denotes a substituted bipyridine or phenanthroline, N-O indicates α-aminoacidate or peptide and O-O represents acetylacetonate or salicylaldehyde. This family of compounds has been evaluated in vitro and in vivo showing cytotoxic, genotoxic, and antineoplastic activity. The action mechanism is still not completely elucidated, but the possibility exists that these compounds interact with DNA by intercalation due to the aromatic moiety. In this work we found, using the properties of the electron density of a π-complex model base-Casiopeína®-base, that the stacking mechanism between Casiopeínas® and DNA bases is due to an electron density deficiency of the ligand of the Casiopeína® which is compensated for by an electron transfer from adenines by a π-π interaction.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1039/c1cp20183b | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
TopoQual polishes circular consensus sequencing data and accurately predicts quality scores.
BMC Bioinformatics
January 2025
Auburn University, Auburn, AL, 36849, USA.
Background: Pacific Biosciences (PacBio) circular consensus sequencing (CCS), also known as high fidelity (HiFi) technology, has revolutionized modern genomics by producing long (10 + kb) and highly accurate reads. This is achieved by sequencing circularized DNA molecules multiple times and combining them into a consensus sequence. Currently, the accuracy and quality value estimation provided by HiFi technology are more than sufficient for applications such as genome assembly and germline variant calling.
View Article and Find Full Text PDFFlap endonuclease 1 repairs DNA-protein cross-links via ADP-ribosylation-dependent mechanisms.
Sci Adv
January 2025
Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA.
DNA-protein cross-links (DPCs) are among the most detrimental genomic lesions. They are ubiquitously produced by formaldehyde (FA), and failure to repair FA-induced DPCs blocks chromatin-based processes, leading to neurodegeneration and cancer. The type, structure, and repair of FA-induced DPCs remain largely unknown.
View Article and Find Full Text PDFPlasmodium falciparum surf4.1 in clinical isolates: From genetic variation and variant diversity to in silico design immunopeptides for vaccine development.
PLoS One
January 2025
Department of Parasitology and Entomology, Faculty of Public Health, Mahidol University, Bangkok, Thailand.
SURFINs protein family expressed on surface of both infected red blood cell and merozoite surface making them as interesting vaccine candidate for erythrocytic stage of malaria infection. In this study, we analyze genetic variation of Pfsurf4.1 gene, copy number variation, and frequency of SURFIN4.
View Article and Find Full Text PDFUntargeted Mutation Triggered by Ribonucleoside Embedded in DNA.
Int J Mol Sci
December 2024
Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
DNA polymerases frequently misincorporate ribonucleoside 5'-triphosphates into nascent DNA strands. This study examined the effects of an incorporated ribonucleoside on untargeted mutations in human cells. Riboguanosine (rG) was introduced into the downstream region of the gene to preferentially detect the untargeted mutations.
View Article and Find Full Text PDFDefects in the Mitochondrial Genome of Dogs with Recurrent Tumours.
Int J Mol Sci
December 2024
Institute of Biological Bases of Animal Production, University of Life Sciences in Lublin, Akademicka 13 St., 20-950 Lublin, Poland.
This study presents a comprehensive analysis of mitochondrial DNA (mtDNA) variations in dogs diagnosed with primary and recurrent tumours, employing Oxford Nanopore Technologies (ONT) for sequencing. Our investigation focused on mtDNA extracted from blood and tumour tissues of three dogs, aiming to pinpoint polymorphisms, mutations, and heteroplasmy levels that could influence mitochondrial function in cancer pathogenesis. Notably, we observed the presence of mutations in the D-loop region, especially in the VNTR region, which may be crucial for mitochondrial replication, transcription, and genome stability, suggesting its potential role in cancer progression.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!