Abstract
Background: End stage renal disease (ESRD) is associated with an increase in oxidative stress, cardiovascular disease and cancer. The main treatment for ESRD is haemodialysis (HD), which itself induces repetitive bouts of oxidative stress through membrane biocompatibility and endotoxin challenge. The resulting higher levels of reactive oxygen species in turn produce increased levels of oxidative DNA damage leading to genomic instability which may influence the higher risk of cancer reported in HD patients. Our aims were to measure levels of oxidative DNA damage in HD patients and in age and gender matched control volunteers. Methods: Thirty eight patients receiving HD in the Western Health and Social Services Trust (WHSCT) and 8 healthy volunteers were recruited. Volunteers gave informed consent and non-fasting morning blood samples were taken and assessed for DNA disruption using the comet assay modified to identify oxidative specific damage. Results: The HD patients had significantly elevated levels of alkaline DNA damage (19.46% ± 1.37% vs 3.86% ± 1.36% tail DNA, p
Highlights
Cardiovascular diseases (CVD) are the leading cause of mortality in patients undergoing haemodialysis (HD) [1]-[3] with an increased frequency of atherosclerosis, heart attacks and strokes, perhaps related to an increase in oxidative stress and damage [4]
HD patients have a very restricted diet and malnutrition occurs in approximately 40% - 50% of cases; this may lead to a restriction or exclusion of certain food categories which may add to the elevated levels of oxidative stress, due to under nutrition and a lack of endogenous antioxidants to combat the elevated levels of ROS [9]
This study reports a significant increase in alkaline and oxidative DNA damage in leucocytes from HD patients compared to the control group
Summary
Cardiovascular diseases (CVD) are the leading cause of mortality in patients undergoing haemodialysis (HD) [1]-[3] with an increased frequency of atherosclerosis, heart attacks and strokes, perhaps related to an increase in oxidative stress and damage [4]. The interaction between the HD patient’s blood and the semipermeable membranes contained in the haemodialysis apparatus increases levels of oxidative stress in these patients [7]. During this interaction, circulating neutrophils are responsible for generating ROS, such as superoxide, which further enhances levels of oxidative stress [8]. The resulting higher levels of reactive oxygen species in turn produce increased levels of oxidative DNA damage leading to genomic instability which may influence the higher risk of cancer reported in HD patients. Conclusion: The significant increase in oxidative DNA damage and the positive correlation with duration of HD treatment and Endo III damage may contribute to the increased cancer risk observed in this patient group. Studies are required to investigate the best way to reduce this damage
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