TY  - JOUR
A1  - Bankoglu, Ezgi Eyluel
A1  - Stipp, Franzisca
A1  - Gerber, Johanna
A1  - Seyfried, Florian
A1  - Heidland, August
A1  - Bahner, Udo
A1  - Stopper, Helga
T1  - Effect of cryopreservation on DNA damage and DNA repair activity in human blood samples in the comet assay
JF  - Archives of Toxicology
N2  - The comet assay is a commonly used method to determine DNA damage and repair activity in many types of samples. In recent years, the use of the comet assay in human biomonitoring became highly attractive due to its various modified versions, which may be useful to determine individual susceptibility in blood samples. However, in human biomonitoring studies, working with large sample numbers that are acquired over an extended time period requires some additional considerations. One of the most important issues is the storage of samples and its effect on the outcome of the comet assay. Another important question is the suitability of different blood preparations. In this study, we analysed the effect of cryopreservation on DNA damage and repair activity in human blood samples. In addition, we investigated the suitability of different blood preparations. The alkaline and FPG as well as two different types of repair comet assay and an in vitro hydrogen peroxide challenge were applied. Our results confirmed that cryopreserved blood preparations are suitable for investigating DNA damage in the alkaline and FPG comet assay in whole blood, buffy coat and PBMCs. Ex vivo hydrogen peroxide challenge yielded its optimal effect in isolated PBMCs. The utilised repair comet assay with either UVC or hydrogen peroxide-induced lesions and an aphidicolin block worked well in fresh PBMCs. Cryopreserved PBMCs could not be used immediately after thawing. However, a 16-h recovery with or without mitotic stimulation enabled the application of the repair comet assay, albeit only in a surviving cell fraction.
KW  - human biomonitoring
KW  - DNA damage
KW  - DNA repair
KW  - comet assay
KW  - blood samples
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-265326
VL  - 95
IS  - 5
ER  - 
TY  - JOUR
A1  - Schupp, Nicole
A1  - Stopper, Helga
A1  - Heidland, August
T1  - DNA Damage in Chronic Kidney Disease: Evaluation of Clinical Biomarkers
JF  - Oxidative Medicine and Cellular Longevity
N2  - 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.
KW  - chronic kidney disease
KW  - cancer risk
KW  - DNA damage
KW  - biomarkers
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-166569
VL  - 2016
IS  - 3592042
ER  - 
TY  - JOUR
A1  - Schupp, Nicole
A1  - Heidland, August
A1  - Stopper, Helga
T1  - Genomic Damage in Endstage Renal Disease - Contribution of Uremic Toxins
N2  - Patients with end-stage renal disease (ESRD), whether on conservative, peritoneal or hemodialysis therapy, have elevated genomic damage in peripheral blood lymphocytes and an increased cancer incidence, especially of the kidney. The damage is possibly due to accumulation of uremic toxins like advanced glycation endproducts or homocysteine. However, other endogenous substances with genotoxic properties, which are increased in ESRD, could be involved, such as the blood pressure regulating hormones angiotensin II and aldosterone or the inflammatory cytokine TNF-. This review provides an overview of genomic damage observed in ESRD patients, focuses on possible underlying causes and shows modulations of the damage by modern dialysis strategies and vitamin upplementation.
KW  - Toxin
KW  - dialysis
KW  - genotoxicity
KW  - uremic toxins
Y1  - 2010
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-68653
ER  -