Effects of long-term ingestion of white tea on oxidation produced by aging and acute oxidative damage in rats.
Cristobal Espinosa RuizLorena CabreraJosé Ángel López-JiménezSalvador ZamoraFrancisca Pérez-LlamasPublished in: Journal of physiology and biochemistry (2017)
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.
Keyphrases
- oxidative stress
- adverse drug
- induced apoptosis
- liver failure
- body weight
- drug induced
- respiratory failure
- dna damage
- hydrogen peroxide
- ischemia reperfusion injury
- aortic dissection
- white matter
- emergency department
- diabetic rats
- low dose
- papillary thyroid
- signaling pathway
- intensive care unit
- blood brain barrier
- brain injury
- mechanical ventilation
- cell cycle arrest
- fatty acid
- replacement therapy
- cell proliferation