alexa Antioxidant effects of tea: evidence from human clinical trials.
Pharmaceutical Sciences

Pharmaceutical Sciences

Biochemistry & Pharmacology: Open Access

Author(s): Rietveld A, Wiseman S

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Abstract Tea remains the most consumed drink in the world after water, well ahead of coffee, beer, wine and carbonated soft drinks. An accumulated number of population studies suggests that consumption of green and black tea beverages may bring positive health effects (1). One hypothesis explaining such effects is that the high levels of flavonoids in tea can protect cells and tissues from oxidative damage by scavenging oxygen-free radicals. Chemically, the flavonoids found in green and black tea are very effective radical scavengers. The tea flavonoids may therefore be active as antioxidants in the digestive tract or in other tissues after uptake. A substantial number of human intervention studies with green and black tea demonstrates a significant increase in plasma antioxidant capacity in humans approximately 1 h after consumption of moderate amounts of tea (1-6 cups/d). There are initial indications that the enhanced blood antioxidant potential leads to reduced oxidative damage to macromolecules such as DNA and lipids. However, the measurement of oxidative damage through biomarkers needs to be further established. In conclusion, tea flavonoids are potent antioxidants that are absorbed from the gut after consumption. Tea consumption consistently leads to a significant increase in the antioxidant capacity of the blood. Beneficial effects of increased antioxidant capacity in the body may be the reduction of oxidative damage to important biomolecules. The scientific support is strongest for the protection of DNA from oxidative damage after black or green tea consumption. However, the quality of the studies now available is insufficient to draw firm conclusions. Therefore, further evidence from human intervention studies is required.
This article was published in J Nutr and referenced in Biochemistry & Pharmacology: Open Access

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