Gadolinium-enhanced cardiac MR exams of human subjects are associated with significant increases in the DNA repair marker 53BP1, but not the damage marker γH2AX

Jennifer S McDonald, Robert McDonald, Jacob B. Ekins, Anthony S. Tin, Sylvain Costes, Tamara M. Hudson, Dana J. Schroeder, Kevin Kallmes, Scott H Kaufmann, Philip M. Young, Aiming Lu, Ramanathan D Kadirvel, David F Kallmes

Research output: Contribution to journalArticle

Abstract

Magnetic resonance imaging is considered low risk, yet recent studies have raised a concern of potential damage to DNA in peripheral blood leukocytes. This prospective Institutional Review Board-approved study examined potential double-strand DNA damage by analyzing changes in the DNA damage and repair markers γH2AX and 53BP1 in patients who underwent a 1.5 T gadolinium-enhanced cardiac magnetic resonance (MR) exam. Sixty patients were enrolled (median age 55 years, 39 males). Patients with history of malignancy or who were receiving chemotherapy, radiation therapy, or steroids were excluded. MR sequence data were recorded and blood samples obtained immediately before and after MR exposure. An automated immunofluorescence assay quantified γH2AX or 53BP1 foci number in isolated peripheral blood mononuclear cells. Changes in foci number were analyzed using the Wilcoxon signed-rank test. Clinical and MR procedural characteristics were compared between patients who had a >10% increase in γH2AX or 53BP1 foci numbers and patients who did not. The number of γH2AX foci did not significantly change following cardiac MR (median foci per cell pre-MR = 0.11, post-MR = 0.11, p = .90), but the number of 53BP1 foci significantly increased following MR (median foci per cell pre-MR = 0.46, post-MR = 0.54, p = .0140). Clinical and MR characteristics did not differ significantly between patients who had at least a 10% increase in foci per cell and those who did not. We conclude that MR exposure leads to a small (median 25%) increase in 53BP1 foci, however the clinical relevance of this increase is unknown and may be attributable to normal variation instead of MR exposure.

Original languageEnglish (US)
Article numbere0190890
JournalPLoS One
Volume13
Issue number1
DOIs
StatePublished - Jan 1 2018

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gadolinium
Gadolinium
Magnetic resonance
DNA repair
Genetic Markers
DNA Repair
Repair
Magnetic Resonance Spectroscopy
DNA
DNA damage
DNA Damage
blood
Blood
radiotherapy
cells
mononuclear leukocytes
magnetic resonance imaging
fluorescent antibody technique
drug therapy
steroids

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this

Gadolinium-enhanced cardiac MR exams of human subjects are associated with significant increases in the DNA repair marker 53BP1, but not the damage marker γH2AX. / McDonald, Jennifer S; McDonald, Robert; Ekins, Jacob B.; Tin, Anthony S.; Costes, Sylvain; Hudson, Tamara M.; Schroeder, Dana J.; Kallmes, Kevin; Kaufmann, Scott H; Young, Philip M.; Lu, Aiming; Kadirvel, Ramanathan D; Kallmes, David F.

In: PLoS One, Vol. 13, No. 1, e0190890, 01.01.2018.

Research output: Contribution to journalArticle

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abstract = "Magnetic resonance imaging is considered low risk, yet recent studies have raised a concern of potential damage to DNA in peripheral blood leukocytes. This prospective Institutional Review Board-approved study examined potential double-strand DNA damage by analyzing changes in the DNA damage and repair markers γH2AX and 53BP1 in patients who underwent a 1.5 T gadolinium-enhanced cardiac magnetic resonance (MR) exam. Sixty patients were enrolled (median age 55 years, 39 males). Patients with history of malignancy or who were receiving chemotherapy, radiation therapy, or steroids were excluded. MR sequence data were recorded and blood samples obtained immediately before and after MR exposure. An automated immunofluorescence assay quantified γH2AX or 53BP1 foci number in isolated peripheral blood mononuclear cells. Changes in foci number were analyzed using the Wilcoxon signed-rank test. Clinical and MR procedural characteristics were compared between patients who had a >10{\%} increase in γH2AX or 53BP1 foci numbers and patients who did not. The number of γH2AX foci did not significantly change following cardiac MR (median foci per cell pre-MR = 0.11, post-MR = 0.11, p = .90), but the number of 53BP1 foci significantly increased following MR (median foci per cell pre-MR = 0.46, post-MR = 0.54, p = .0140). Clinical and MR characteristics did not differ significantly between patients who had at least a 10{\%} increase in foci per cell and those who did not. We conclude that MR exposure leads to a small (median 25{\%}) increase in 53BP1 foci, however the clinical relevance of this increase is unknown and may be attributable to normal variation instead of MR exposure.",
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