Elitsa Stoyanova

Medical University of Sofia

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Ricard Marcos

Universitat Autònoma de Barcelona

Susana Pastor

Universitat Autònoma de Barcelona

José Ballarín

Puigvert Foundation

Elisabet Coll

Puigvert Foundation

Lara Rodríguez‐Ribera

Universitat Autònoma de Barcelona

Elisabeth Coll

Organización Nacional de Trasplantes

Silvia B. Sandoval

Universitat Autònoma de Barcelona

Zuray Corredor

Universidad Cooperativa de Colombia

Irene Silva

Universitat Autònoma de Barcelona

Juan Manuel Díaz

Western University

Cooperative Institutions

Universitat Autònoma de Barcelona

Puigvert Foundation

Medical University of Sofia

Sofia University "St. Kliment Ohridski"

Bulgarian Academy of Sciences

Instituto de Salud Carlos III

Medical University Pleven

Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública

Universitat de Barcelona

Centro de Investigación Biomédica en Red

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Genomic instability in chronic renal failure patients

Environmental and Molecular Mutagenesis (2012)

Silvia B. Sandoval Susana Pastor Elitsa Stoyanova Lara Rodríguez‐Ribera Wilser Andrés García-Quispes

Abstract Patients suffering chronic renal failure (CRF) exhibit a high incidence of cancer, as well as high levels of genetic damage. We hypothesized that these patients show genomic instability as measured by increased radiosensitivity to the induction of genetic damage. The background levels of genetic damage and the net genetic damage after in vitro irradiation with 0.5 Gy were analyzed using the micronucleus assay in peripheral blood lymphocytes of 174 CRF patients and 53 controls. The net radiation‐induced genetic damage was significantly higher in CRF patients with respect to controls. Among CRF patients, the levels of genetic damage were higher in those with prior incidence of cancer than in those without cancer; in addition, those CRF patients undergoing hemodialysis presented with higher levels of genetic damage than those in the advanced Stages (4–5) of the pathology. A positive association was observed between basal and net micronucleus frequency among CFR patients. However, no association was found between net genetic damage and parameters linked to the different stages of the pathology, such as urine creatinine levels and glomerular filtration rate. Our results indicate that CRF patients show increased radiosensitivity and that the degree of radiosensitivity is associated with the progression of the pathological stage of the disease. Environ. Mol. Mutagen., 2012. © 2012 Wiley Periodicals, Inc.

Radiosensitivity

Genetic predisposition

10.1002/em.21694

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Citations (26)

Oxidative DNA damage in chronic renal failure patients

Nephrology Dialysis Transplantation (2009)

Elitsa Stoyanova Silvia B. Sandoval Liliana Zúñiga Naouale El Yamani Elisabeth Coll

Background: Chronic renal failure (CRF) patients present a high incidence of cardiovascular pathologies and cancer. This has been attributed to the existence of genomic instability in these patients, and consequently they should present elevated levels of genetic damage.

Comet Assay

10.1093/ndt/gfp575

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Citations (57)

Enzymatically degraded low density lipoproteins are more potent inducers of egr-1 mRNA than oxidized or native low density lipoproteins

Clinical Biochemistry (2001)

Elitsa Stoyanova Anthony M. Tesch Victor W. Armstrong Eberhard Wieland

Inducer

10.1016/s0009-9120(01)00258-2

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Citations (5)

Molecular mechanisms in skin micro-blood vessel structural changes under cold microwave argon plasma exposure—in vivo, pilot study

Biophysical Journal (2024)

Lubomir Traikov Todor Bogdanov Katherina Smejkalova Todor Hikov Maria Dimitrova

Vasomotion

Regenerative Medicine

10.1016/j.bpj.2023.11.232

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Citations (0)

BPS2025 - Dynamic fluidic perturbation flows promote biomechanical restructuration of the micro-vasculature bed and stimulation of neo-angiogenesis during the action of cold microwave argon plasma in mice in vivo

Biophysical Journal (2025)

Lubomir Traikov Todor Bogdanov M. Dimitrova Elitsa Stoyanova Radka Tafradjiiska-Hadjiolova

Fluidics

10.1016/j.bpj.2024.11.3239

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Influence of Carnicor, Venofer, and Sevelamer on the levels of genotoxic damage in end‐stage renal disease patients

Environmental and Molecular Mutagenesis (2018)

Susana Pastor Elisabeth Coll Lara Rodríguez‐Ribera Elitsa Stoyanova Zuray Corredor

End‐stage renal disease (ESRD) patients present high levels of phosphorus and calcium products in serum, which contribute to the development of vascular calcification and cardiovascular disease, and to low iron stores and carnitine deficiency. For these reasons, ESRD patients are generally supplemented with different medicines. Some of the most common treatments include the use of Carnicor, Venofer, and Sevelamer drugs. Carnicor is used as a source of L‐carnitine, acting as antioxidant and neuroprotector. Venofer is used to reduce the deficit of iron. Sevelamer is used to treat hyperphosphatemia. To determine the potential harmful genotoxic effects of these drugs, a group of 214 patients included in a hemodialysis program with different intakes of Carnicor, Venofer, and Sevelamer were evaluated. The levels of basal and oxidative DNA damage, as well as chromosomal damage, were measured in all individuals using the comet and the micronucleus assays, respectively. Our results indicate that Carnicor administration was associated with low but significant increases in the frequency of basal DNA damage and micronuclei. Environ. Mol. Mutagen. 59:302–311, 2018. © 2018 Wiley Periodicals, Inc.

Sevelamer

10.1002/em.22170

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Genetic damage in chronic renal failure patients is associated with the glomerular filtration rate index

Mutagenesis (2010)

Silvia B. Sandoval Elitsa Stoyanova Elisabeth Coll Susana Pastor J. Rivera Reyes

Chronic renal failure (CRF) patients are considered to present genomic instability and, as a consequence, elevated levels of genetic damage. An open question is whether this damage is related to the stage of the pathology. To determine the background levels of genetic damage, a large population of 258 Caucasian adults (201 CRF patients and 57 controls) was analysed using the micronucleus (MN) assay. The frequency of MN in CRF patients was significantly higher than in controls and correlated with the progression of the disease, according to the glomerular filtration rate. In addition, a significant association was observed between genetic damage and serum creatinine levels. Genetic damage, measured as frequency of MN, increases when renal function decreases. The fact that an increased level of MN is already observed in patients' Stage 2 seems to indicate a genetic predisposition on these patients. Nevertheless, part of the observed damage can be attributed to the uraemic state itself.

Genetic predisposition

Chronic renal failure

10.1093/mutage/geq047

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Citations (29)

GLOMERULAR FILTRATION RATE INDEX IS ASSOCIATED WITH GENETIC DAMAGE IN CHRONIC RENAL FAILURE PATIENTS

Silvia B. Sandoval Elitsa Stoyanova Elisabeth Coll

Chronic renal failure

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Citations (3)

Base excision repair capacity in chronic renal failure patients undergoing hemodialysis treatment

Cell Biochemistry and Function (2013)

Elitsa Stoyanova Susana Pastor Elisabet Coll Amaya Azqueta Andrew Collins

The aim of this study was to determine if the differences observed in the levels of DNA damage in a group of patients suffering from chronic renal failure are due to differences in the repair capability. DNA damage was initially measured with the comet assay in 106 hemodialysis patients. A selected group of 21 patients representing high (ten patients) and low (11 patients) levels of DNA damage were obtained for determination of base excision repair capacity. This was measured in an in vitro assay where protein extracts from lymphocytes were incubated with a substrate of DNA containing 8‐oxoguanine, and the rate of incision was measured with the comet assay. Patients with high levels of genomic damage showed, as an average, significantly lower repair capacity (12·73 ± 1·84) in comparison with patients with low levels of genomic damage (18·13 ± 1·13). Nevertheless, the correlation coefficient between repair ability and levels of genomic damage was found to be only close to the significance value ( r :−0·423, p : 0·056). Although DNA damage was clearly related to time on hemodialysis, base excision repair capacity was not. This is one of the few studies providing information on the repair capacity of chronic renal failure patients undergoing hemodialysis. As a summary, our results would indicate that DNA damage levels are in part associated to the repair capacity of the patients, and this repair capacity is not associated with the duration of hemodialysis treatment. Copyright © 2013 John Wiley & Sons, Ltd.

Comet Assay

Chronic renal failure

10.1002/cbf.2989

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Citations (21)

Time in hemodialysis modulates the levels of genetic damage in hemodialysis patients

Environmental and Molecular Mutagenesis (2014)

Lara Rodríguez‐Ribera Elitsa Stoyanova Zuray Corredor Elisabet Coll Irene Silva

It is assumed that hemodialysis treatment can diminish the levels of genetic damage in circulating lymphocytes by cleaning the blood of uremic toxins that cause oxidative stress. However, the hemodialysis process by itself may also induce genomic damage by producing reactive oxygen species (ROS). We conducted a follow‐up study in a group of 70 hemodialysis patients followed for a mean time of 15 months. We investigated the effect of exposure time in hemodialysis on the levels of genetic damage in peripheral blood lymphocytes using the micronucleus assay. In addition, genetic damage after in vitro irradiation with 0.5 Gy was also analyzed to evaluate changes in radiosensitivity. Our results showed that, at the end of the study, there was a decrease in both the basal levels of genetic damage (9.9 ± 1.0 vs. 7.6 ± 0.7) and radiosensitivity values (38.5 ± 3.0 vs. 27.6 ± 2.4). We conclude that hemodialysis procedures may act as an ameliorating factor reducing the genetic damage present in chronic kidney disease patients. Environ. Mol. Mutagen. 55:363–368, 2014. © 2014 Wiley Periodicals, Inc.

Radiosensitivity

Radioresistance

10.1002/em.21849

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Citations (12)