Abstract
The infusion tea extracted from the leaves of the plant Camellia sinensis can be used in the prevention of cancer, cardiovascular and neurodegenerative diseases, and aging, while adriamycin (ADR) is an anticancer drug that increases oxidative stress in cells. The present study evaluated the protective effect of the long-term consumption of white tea used at two different doses against the oxidative stress produced by aging and acute oxidation caused ADR treatment. At wearing, rats received distilled water (control), or 0.15 (dose 1) or 0.45 mg (dose 2) of solid tea extract/kilogram body weight in their drink. At 12 months, about half of the rats of each group were injected with a bolus of ADR, and six rats of the control group with an injection of saline solution and sacrificed. The rest of the animals continued in their cages until 24 months of age, when they were sacrificed. Lipid and protein oxidation of liver and brain microsomes was analyzed by measuring hydroperoxide and carbonyl levels. White tea consumption for 12 months at a non-pharmacological dose was seen to reverse the oxidative damage caused by ADR in both liver and brain, while the consumption of white tea for 20 months at a non-pharmacological dose had no effect on carbonyl or hydroperoxides in these tissues. The long-term ingestion of white tea protected tissues from acute oxidative stress but did not affect chronic oxidative agents such aging.
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Acknowledgements
This study was funded by “Ministerio de Ciencia y Tecnología” of Spain with the project AGL2005-08088-C02-01 and Beca FPU (AP2006-02642). The authors would like to thank Mª Pilar Almajano for extract of the white tea and Rebeca Martinez-Tomás and Daniel Gonzalez for technical support.
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All the study protocols were in accordance with the Helsinki Declaration and were approved under supervision of the Bioethical Committee of the Murcia University, Spain.
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Espinosa Ruiz, C., Cabrera, L., López-Jiménez, J.Á. et al. Effects of long-term ingestion of white tea on oxidation produced by aging and acute oxidative damage in rats. J Physiol Biochem 74, 171–177 (2018). https://doi.org/10.1007/s13105-017-0591-z
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DOI: https://doi.org/10.1007/s13105-017-0591-z