Urinary level of 1,N(6) -ethenodeoxyadenosine, a marker of oxidative stress, is associated with salt excretion and omega 6-polyunsaturated fatty acid intake in postmenopausal Japanese women.

Tomoyuki Hanaoka, Jagadeesan Nair, Yoshiko Takahashi, Satoshi Sasaki, Helmut Bartsch, Shoichiro Tsugane

Index: Int. J. Cancer 100(1) , 71-5, (2002)

Full Text: HTML

Abstract

Excretion of 1,N(6)-ethenodeoxyadenosine (epsilon dA), a marker for lipid peroxidation (LPO)-derived DNA damage was analyzed in urine of nonsmoking postmenopausal women participating in a dietary intervention trial in Northern Japan. Hereby the efficacy of dietary consultation in reducing salt and increasing vitamin C and carotenes during 1 year was estimated. Thirty postmenopausal women, 60-69 years of age, from the intervention group and 30 age-matched women from the control group were randomly selected. The subjects completed a self-administered diet history questionnaire and in the pre- and post-intervention period 48 hr urine and fasting blood samples were collected. epsilon dA in urine was analyzed by an immuno-precipitation-high performance liquid chromatography-fluorescence detection method. epsilon dA excretion (/48 hr) in the 59 postmenopausal Japanese women with complete urine collection ranged from 12-226 pmol at the pre-intervention. At the pre-intervention, epsilon dA excretion was positively associated with urinary salt excretion (R = 0.33, p = 0.01) and omega-6 polyunsaturated fatty acid intake (%energy value, R = 0.28, p = 0.03) in the 59 women. The average epsilon dA excretion in the intervention group was 61 pmol at pre-intervention and 44 pmol at post-intervention (p = 0.14). In the control group, it was 58 pmol at pre-intervention and 75 pmol at post-intervention (p = 0.24). During the intervention period, 18/29 (62%) of the subjects in the intervention group exhibited the decreased excretion and 10/26 (38%) in the control group (p = 0.08). Results from this pilot study suggest urinary epsilon dA as a potential biomarker of DNA damage possibly derived from salt-induced inflammation and LPO; further exploration of epsilon dA in human biomonitoring studies is warranted.Copyright 2002 Wiley-Liss, Inc.