Patients with chronic kidney disease (CKD) exhibit an increased cancer risk compared to a healthy control population. To be able to estimate the cancer risk of the patients and to assess the impact of interventional therapies thereon, it is of particular interest to measure the patients' burden of genomic damage. Chromosomal abnormalities, reduced DNA repair, and DNA lesions were found indeed in cells of patients with CKD. Biomarkers for DNA damage measurable in easily accessible cells like peripheral blood lymphocytes are chromosomal aberrations, structural DNA lesions, and oxidatively modified DNA bases. In this review the most common methods quantifying the three parameters mentioned above, the cytokinesis-block micronucleus assay, the comet assay, and the quantification of 8-oxo-7,8-dihydro-2'-deoxyguanosine, are evaluated concerning the feasibility of the analysis and regarding the marker's potential to predict clinical outcomes.
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http://dx.doi.org/10.1155/2016/3592042 | DOI Listing |
Dalton Trans
January 2025
Department of Chemistry, Faculty of Science, Cairo University, Gamma Street, Giza, Cairo 12613, Egypt.
The photo-induced CO-releasing properties of the dark-stable complex [RuCl(CO)L] (L = 2-(pyridin-2-yl)quinoxaline) were investigated under 468 nm light exposure in the presence and absence of biomolecules such as histidine, calf thymus DNA and hen egg white lysozyme. The CO release kinetics were consistent regardless of the presence of these biomolecules, suggesting that they did not influence the CO release mechanism. The quinoxaline ligand demonstrated exceptional cytotoxicity against human acute monocytic leukemia cells (THP-1), with evidence of potential DNA damage ascertained by comet assay, while it remained non-toxic to normal kidney epithelial cells derived from African green monkey (Vero) cell lines.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Case Western Reserve University, Cleveland, OH, USA.
Background: Even when patients carry disease-causing mutations their entire lives, they do not develop Alzheimer's disease (AD) until later in life. The reason for this loss of brain resilience is not known, and two of the greatest risk factors for developing AD are aging and traumatic brain injury (TBI). Unfortunately, there are currently no protective treatments for patients that prevent the development of AD.
View Article and Find Full Text PDFBackground: UFMylation is an understudied ubiquitin-like post-translational modification (PTM). Like ubiquitin, UFM1 is conjugated to substrates via a catalytic cascade involving a UFM1-specific E1 (UBA5), E2 (UFC1), and an E3 ligase complex (UFL1, DDRGK1 and CDK5RAP3). UFMylation is reversible, and this is mediated by UFSP2.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Pennsylvania, Philadelphia, PA, USA.
Background: To date, Alzheimer's disease (AD) research has principally focused on neurons. In contrast, recent studies suggest that genetic mechanisms drive microglia towards prolonged inflammation in AD brains, exacerbating neurodegeneration. Indeed, many of the 70 disease-associated loci uncovered with genome-wide association studies (GWAS) reside near genes related to microglial function, such as TREM2.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Texas Medical Branch, Galveston, TX, USA.
Background: The oligomers and fibrils of tau are well known as an indicator of Alzheimer's disease (AD). Recently, other protein aggregates have been shown to be potentially involved in the development of the disease. One of these proteins is p53, involved in DNA repair.
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