Latin Name: Camellia sinensis
Pol Merkur Lekarski. 2005 Jul;19(109):41-7
[Effect of tea polyphenols on oxidative metabolism of polymorphonuclear neutrophils in healthy and obese people][Article in Polish]
Zielińska-Przyjemska M, Dobrowolska-Zachwieja A.
Akademia Medyczna im. Karola Marcinkowskiego w Poznaniu, Zakład Biochemii Katedry Biochemii Farmaceutycznej. firstname.lastname@example.org
Obese people are at high risk for developing diabetes, dyslipidemia, hypertension, and cardiovascular diseases, which lead to an increased risk of mortality. Evidence for the potential role of oxidative stress in various diseases and pathophysiological processes suggests that the dietary intake and the therapeutic use of antioxidants may have positive health effects. The aim of the study was: 1) to investigate the ability of the major tea polyphenols: (-)-epigallocatechin gallate (EGCG), theaflavins (TF) and gallic acid (GA) to protect in vitro human neutrophils from oxidative damage induced by phorbol myristate acetate (PMA), 2) estimation the level of reactive oxygen species (ROS) production in obese patient depending on the red tea Pu-Erh drinking, 3) estimation inflammatory marker: CRP. MATERIAL AND METHODS: We tested 14 obese patients (aged 45+/-12 years, women, BMI=34+/-5.1 kg/m2). The inclusion criteria were based on physical examination, BMI, WHR, and the body composition examination based on bioimpedance method. PMA were isolated and oxidant production, in response to 1 microg/ml PMA, was characterized by the production of hydrogen peroxide, nitric oxide and chemiluminescence intensity. CRP level was assayed by the immunoturbidimetric test in serum. Control group consisted of healthy blood donors. RESULTS: Women consuming red tea revealed alteration in reactive oxygen species generation; the relative decrease of RFT was greater after 5 months than that after 1 month of treatment. A decrease in ROS generation after red tea consumption was accompanied by the decrease of ROS in response to tested compounds in normal cells. EGCG and TF showed similar potency in antioxidative activities. Tea polyphenols were not found to modulate CRP level in obese women. CONCLUSIONS: Tea may thus represent an important source of dietary antioxidants; there is need for more detailed studies to improve our understanding of the role of tea in reducing risk of major disease states.
Phytother Res. 2009 Mar 10
Protective action of aqueous black tea (Camellia sinensis) extract (BTE) against ovariectomy-induced oxidative stress of mononuclear cells and its associated progression of bone loss.
Das AS, Mukherjee M, Das D, Mitra C.
Department of Physiology, Presidency College, Kolkata 700 073, India.
The protective action of aqueous black tea extract (BTE) against ovariectomy-induced oxidative stress of mononuclear cells and its associated progression of bone loss was demonstrated in this study. Eighteen female adult 6-month-old Wistar albino rats were divided into three groups: sham-control (A), bilaterally ovariectomized (B) and bilaterally ovariectomized + BTE supplemented (C). Studies included the measurement of oxidative (nitric oxide, lipid peroxidation) and antioxidative (superoxide dismutase, catalase) markers, inflammatory cytokines (IL-6, TNF-alpha), osteoclast differentiation factor (RANKL) and bone resorption markers (tartrate-resistant acid phosphatase and hydroxyproline). Also quantitative histomorphometry and histological studies were undertaken. The bone breaking force was measured. The results indicate that BTE was effective in preserving and restoring skeletal health by reducing the number of active osteoclasts. Such changes with BTE supplementation were steadily linked with the reduced oxidative stress of mononuclear cells, serum levels of bone resorbing cytokines, osteoclast differentiation factor and resorption markers. The results of the bone breaking force, histological and histomorphometric analyses further supported the hypothesis. This study suggests that BTE has both protective and restorative actions against ovariectomy-induced mononuclear cell oxidative stress and associated bone loss. Copyright (c) 2009 John Wiley & Sons, Ltd.