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February 28-March 01, 2019 | Paris, France
Palliative Care, Obstetrics and Gynecology
Stroke and Clinical Trials
International Conference on
Joint Event on
International Conference on
&
Journal of Research and Reports in Gynecology and Obstetrics | Volume: 3
Oxidative DNA damage is elevated in renal patients undergoing haemodialysis
Mary Hannon-Fletcher
Ulster University, UK
E
ndstagerenal disease (ESRD) isassociatedwithan increase in
oxidative stress, cardiovascular diseaseandcancer. Themain
treatment for ESRD, haemodialysis (HD), 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. We measured
levels of oxidative DNA damage insss thirty-eight patients
receiving HD in the Western Health and Social Services Trust
(WHSCT), and 8 age and gender matched control volunteers.
Volunteers gave informed consent and non-fasting morning
blood samples were taken and assessed for DNA damage
using the Modified Comet to identify oxidative specific damage
by introducing an enzymatic step with the bacterial enzymes
endonuclease III (Endo III, recognise pyrimidine-pyrimidine
breaks) and formamidepyrimidine DNA glycosilase (FPG,
recognise purine-purine breaks. The study then continued into
a 3-month intervention with a novel supplement to determine
if levels of oxidative damage could be reduced with this novel
supplement. The HD patients had significantly elevated levels
of alkaline DNA damage (19.46 ± 8.35 vs 3.86 ± 0.99 % tail DNA,
p<0.05) and oxidative DNA damage formamidepyrimidine DNA
glycosilase (5.81 ± 6.63 vs 1.23 ± 0.39 % tail DNA, p<0.0) and
endonuclease III (6.04 ± 6.11 vs 1.98 ± 0.85% tail DNA, p<0.01)
compared to controls, respectively. A positive correlation was
observed between the duration on dialysis (months) and levels
of Endo III specific damage (p=0.041). Following the 3-month
intervention we observed a significant reduction in Alkaline,
EndoIII and FPG DNA damage in the HD treatment group, while
the HD placebo group had DNA damage levels significantly
increased from baseline at 3 months. We conclude, 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. In addition, treatment with a novel supplement
significantly reduced DNA damage in the HD treatment group
and could be recommend as a routine treatment in HD patients.
Speaker Biography
Mary Hannon-Fletcher is currently a senior lecturer in Biomedical Sciences at Ulster
University and a member of the Biomedical Sciences Research Institute. Having re-
joined the School after holding the position of Head of School of Health Sciences for 6
years, where she led a multi- professional team of Allied Health Professions (AHP’s) and
Healthcare Scientists. Professionally she holds a First Class (Hons) BSc in Biomedical
Sciences (1995) and a PhD in Biomedical Sciences, 2000, from Ulster University. She
is a Fellow of the Institute of Biomedical Sciences (FIBMS); Chartered Scientist (CSi);
Registered Biomedical Scientist with the Health and Care Professions Council (HCPC)
and Fellow of the Higher Education Academy (FHEA).
e:
mp.hannon@ulster.ac.ukMary Hannon-Fletcher
, Res Rep Gynaecol Obstet, Volume 3
DOI: 10.4066/2591-7366-C1-002