DNA repair and recovery of RNA synthesis in uremic patients

Malachi, Tsipora; Zevin, D; Gafter, Uzi; Chagnac, Avry; Slor, Hanoch; Levi, J

doi:10.1038/ki.1993.256

Cited by 75 publications

(32 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Surprisingly, the short-term-hemodialysis groups of our study (less than 3 months and 3-12 months renal replacement therapy) even showed increased DNA repair compared with control subjects, while DNA repair of patients with medium-duration dialysis therapy (60 months) was comparable to controls. These latter data fit well to similar results from Israel in MHD patients treated for an average of 45 months [91,92]. In contrast, in patients with nondialyzed chronic renal failure, decreased DNA repair was found [92].…”

Section: Impaired Dna Repair After Long-term Hemodialysis Treatmentsupporting

confidence: 78%

Cancer in End-Stage Renal Disease: Potential Factors Involved

Vamvakas

Bahner²,

Heidland³

1998

Am J Nephrol

166

113

View full text Add to dashboard Cite

Increased incidence of cancer at various sites is observed in patients with end-stage renal disease (ESRD). In particular, lymphomas and carcinomas of the kidney, prostate, liver and uterus show an enhanced prevalence in these subjects compared with the general population. A multitude of factors directly or indirectly associated with the renal disease and the treatment regimens may contribute to the increased tumor formation in these patients. Impaired function of the immune system and of DNA repair mechanisms as well as reduced antioxidant defense, accumulation of carcinogenic compounds partly due to reduced renal elimination as well as chronic infections and inflammations are found more frequently in patients with ESRD compared with the general population and may act in concert to accelerate malignant transformation and tumor formation.

show abstract

Section: Impaired Dna Repair After Long-term Hemodialysis Treatmentsupporting

confidence: 78%

Cancer in End-Stage Renal Disease: Potential Factors Involved

Vamvakas

Bahner²,

Heidland³

1998

Am J Nephrol

166

113

View full text Add to dashboard Cite

show abstract

“…The complication of clonal emergence may increase the chance that a clinically silent primary or controllable/reversible secondary hyperplasia becomes a clinically important disease that requires surgery. It is also possible that an impaired capacity for DNA repair, which has been described in uremic patients (32,33), further increases the likelihood of clonal transformation in their parathyroid glands.…”

Section: Dna Sample Preparationmentioning

confidence: 99%

Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia.

Arnold¹,

Brown²,

Ureña³

et al. 1995

J. Clin. Invest.

374

144

View full text Add to dashboard Cite

The pathogeneses of parathyroid disease in patients with uremia and nonfamilial primary parathyroid hyperplasia are poorly understood. Because of multigland involvement, it has been assumed that these common diseases predominantly involve polyclonal (non-neoplastic) cellular proliferations, but an overall assessment of their clonality has not been done. We examined the clonality of these hyperplastic parathyroid tumors using X-chromosome inactivation analysis with the M27,B (DXS255) DNA polymorphism and by searching for monoclonal allelic losses at M27f3 and at loci on chromosome band 11q13. Fully 7 of 11 informative hemodialysis patients (64%) with uremic refractory hyperparathyroidism harbored at least one monoclonal parathyroid tumor (with a minimum of 12 of their 19 available glands being monoclonal). Tumor monoclonality was demonstrable in 6 of 16 informative patients (38%) with primary parathyroid hyperplasia. Histopathologic categories of nodular versus generalized hyperplasia were not useful predictors of clonal status. These observations indicate that monoclonal parathyroid neoplasms are common in patients with uremic refractory hyperparathyroidism and also develop in a substantial group of patients with sporadic primary parathyroid hyperplasia, thereby changing our concept of the pathogenesis of these diseases. Neoplastic transformation of preexisting polyclonal hyperplasia, apparently due in large part to genes not yet implicated in parathyroid tumorigenesis and possibly including a novel X-chromosome tumor suppressor gene, is likely to play a central role in these disorders. (J. Clin. Invest. 1995. 95

show abstract

“…It is of note that UV irradiation-induced DNA repair in PBMC exhibited a similar pattern, i.e. DNA repair increased significantly following HD [7, 8]. …”

Section: Discussionmentioning

confidence: 97%

Spontaneous DNA Repair Increases during Hemodialysis

Herman

Ori²,

Chagnac³

et al. 2008

Nephron Clin Pract

Self Cite

View full text Add to dashboard Cite

Background: Hemodialysis (HD) patients are subjected to increased oxidative stress. Oxidative stress causes DNA damage, which may be repaired by a DNA repair system. ‘Spontaneous DNA repair’ expresses DNA repair of in vitro unstimulated cells. The aim of the study was to evaluate the effect of one HD session on spontaneous DNA repair in peripheral blood mononuclear cells (PBMC). Methods: PBMC were separated from blood samples for the determination of spontaneous DNA repair, measured by ³H-thymidine incorporation, before and immediately after one HD session. Percent double-stranded DNA (ds-DNA) was measured by the fluorometric assay of DNA unwinding (FADU). Results: DNA repair increased significantly following HD. To examine if this increase was caused by newly produced DNA damage, we studied the effect of HD on percent ds-DNA in PBMC. HD significantly reduced percent ds-DNA, indicating increased DNA breakage. By repeating FADU in the presence of formamidopyrimidine-DNA glycosylase (Fpg), which nicks DNA at oxidized purine sites, we could show that the increased DNA damage was caused by oxidation. Conclusion: Spontaneous DNA repair increases during HD in response to an increase in DNA damage induced by oxidative stress.

show abstract

DNA repair and recovery of RNA synthesis in uremic patients

Cited by 75 publications

References 26 publications

Cancer in End-Stage Renal Disease: Potential Factors Involved

Cancer in End-Stage Renal Disease: Potential Factors Involved

Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia.

Spontaneous DNA Repair Increases during Hemodialysis

Contact Info

Product

Resources

About