Send to

Choose Destination
Mol Nutr Food Res. 2014 Jun;58(6):1379-83. doi: 10.1002/mnfr.201300751. Epub 2014 Feb 28.

Effects of single dose and regular intake of green tea (Camellia sinensis) on DNA damage, DNA repair, and heme oxygenase-1 expression in a randomized controlled human supplementation study.

Author information

Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong.


Regular intake of green tea (Camellia sinensis) lowers DNA damage in humans, but molecular mechanisms of genoprotection are not clear. Protection could be via direct antioxidant effects of tea catechins, but, paradoxically, catechins have pro-oxidant activity in vitro, and it is hypothesized that mechanisms relate to redox-sensitive cytoprotective adaptations. We investigated this hypothesis, focusing particularly on effects on the DNA repair enzyme human oxoguanine glycosylase 1 (hOGG1), and heme oxygenase-1, a protein that has antioxidant and anti-inflammatory effects. A randomized, placebo-controlled, human supplementation study of crossover design was performed. Subjects (n = 16) took a single dose (200 mL of 1.5%, w/v) and 7-days of (2 × 200 mL 1%, w/v per day) green tea (with water as control treatment). Lymphocytic DNA damage was ∼30% (p < 0.001) lower at 60 and 120 min after the single dose and in fasting samples collected after 7-day tea supplementation. Lymphocytic hOGG1 activity was higher (p < 0.0001) at 60 and 120 min after tea ingestion. Significant increases (p < 0.0005) were seen in hOGG1 activity and heme oxygenase-1 after 7 days. Results indicate that molecular triggering of redox-sensitive cytoprotective adaptations and posttranslational changes affecting hOGG1 occur in vivo in response to both a single dose and regular intake of green tea, and contribute to the observed genoprotective effects of green tea.


DNA damage and repair; Green tea; Heme oxygenase-1; Redox tone; hOGG1

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center