Oxidative DNA damage during sleep periods among nightshift workers.
Oxidative DNA damage may be increased among nightshift workers because of suppression of melatonin, a cellular antioxidant, and/or inflammation related to sleep disruption. However, oxidative DNA damage has received limited attention in previous studies of nightshift work.



From two previous cross-sectional studies, urine samples collected during a night sleep period for 217 dayshift workers and during day and night sleep (on their first day off) periods for 223 nightshift workers were assayed for 8-hydroxydeoxyguanosine (8-OH-dG), a marker of oxidative DNA damage, using high-performance liquid chromatography with electrochemical detection. Urinary measures of 6-sulfatoxymelatonin (aMT6s), a marker of circulating melatonin levels, and actigraphy-based sleep quality data were also available.



Nightshift workers during their day sleep periods excreted 83% (p=0.2) and 77% (p=0.03) of the 8-OH-dG that dayshift workers and they themselves, respectively, excreted during their night sleep periods. Among nightshift workers, higher aMT6s levels were associated with higher urinary 8-OH-dG levels, and an inverse U-shaped trend was observed between 8-OH-dG levels and sleep efficiency and sleep duration.



Reduced excretion of 8-OH-dG among nightshift workers during day sleep may reflect reduced functioning of DNA repair machinery, which could potentially lead to increased cellular levels of oxidative DNA damage. Melatonin disruption among nightshift workers may be responsible for the observed effect, as melatonin is known to enhance repair of oxidative DNA damage. Quality of sleep may similarly impact DNA repair. Cellular levels of DNA damage will need to be evaluated in future studies to help interpret these findings.
Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Parveen
P
Bhatti
Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Dana K
DK
Mirick
Program in Biostatistics and Biomathematics, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Timothy W
TW
Randolph
Duke University, Nicholas School of the Environment and Duke Global Health Institute, Durham, North Carolina, USA.
Jicheng
J
Gong
Department of Biobehavioral Nursing and Health Systems, School of Nursing, University of Washington, Seattle, Washington, USA.
Diana Taibi
DT
Buchanan
Duke University, Nicholas School of the Environment and Duke Global Health Institute, Durham, North Carolina, USA.
Junfeng Jim
JJ
Zhang
Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Scott
S
Davis
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D015415:Biomarkers / Q000652:urine; D002940:Circadian Rhythm; D003430:Cross-Sectional Studies; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D005260:Female; D006801:Humans; D008297:Male; D008550:Melatonin / Q000031:analogs & derivatives / Q000652:urine; D008875:Middle Aged; D016273:Occupational Exposure / Q000009:adverse effects*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D012890:Sleep / Q000502:physiology*; D014940:Work Schedule Tolerance; D055815:Young Adult
D015415:Biomarkers; C054513:6-sulfatoxymelatonin; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine; D008550:Melatonin