Urinary level of 1,N6 -ethenodeoxyadenosine, a marker of oxidative stress, is associated with salt excretion and ω6-polyunsaturated fatty acid intake in postmenopausal Japanese women
✍ Scribed by Tomoyuki Hanaoka; Jagadeesan Nair; Yoshiko Takahashi; Satoshi Sasaki; Helmut Bartsch; Shoichiro Tsugane
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- French
- Weight
- 106 KB
- Volume
- 100
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
Abstract
Excretion of 1,N^6^‐ethenodeoxyadenosine (ϵdA), 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. ϵdA in urine was analyzed by an immuno‐precipitation‐high performance liquid chromatography‐fluorescence detection method. ϵdA 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, ϵdA excretion was positively associated with urinary salt excretion (R = 0.33, p = 0.01) and ω‐6 polyunsaturated fatty acid intake (%energy value, R = 0.28, p = 0.03) in the 59 women. The average ϵdA 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 ϵdA as a potential biomarker of DNA damage possibly derived from salt‐induced inflammation and LPO; further exploration of ϵdA in human biomonitoring studies is warranted. © 2002 Wiley‐Liss, Inc.