mental-health

Author: Feng Li and Juan Xu and Jing Zhou and Liyan Zhao and Jianchun Sheng and Guiju Sun and Qiuhui Hu

The anticlastogenic effect of micrometer powder of selenium-enriched green tea (MSTP) was evaluated by using a chromosomal aberration assay in mouse testicular cells. Animals fed with a Se-deficient diet were treated with MSTP, micrometer powder of regular green tea (MRTP), selenite, and MRTP + selenite for 30 days by an intragastric route, followed by treatment of mitomycin C (MMC) on day 19 through intraperitoneal injection (ip). Selenium status and antioxidant enzymes were measured. Results indicated that MSTP showed a significant capability to reduce the incidence of MMC-induced chromosomal aberrations in spermatocytes from 22.7% to 6.7%. This inhibitory was highest, for MSTP, at 73.1%, while it was only 38.4% for MRTP. After 30 days of a Se-deficient diet, mice, either with or without the MMC treatment, showed a lower selenium concentration in blood and liver as well as lower enzyme activity of the antioxidants, GPx and SOD. Supplementation with MSTP, selenite, or selenite + MRTP enhanced the activities of these antioxidant enzymes. This enhancement was accompanied with a concomitant elevation of selenium levels, which favored the synthesis of the seleno-enzyme GPx and protected the cells from the MMC-induced oxidative stress. Our results indicate that MSTP is both able to prevent the chromosomal aberrations induced by MMC in mouse spermatocytes and to enhance GPx and SOD activity in blood serum and liver.

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Author: Chwan-Li Shen and James K. Yeh and Jay J. Cao and Jia-Sheng Wang

Osteoporosis is a major health problem in both elderly women and men. Epidemiological evidence has shown an association between tea consumption and the prevention of age-related bone loss in elderly women and men. Ingestion of green tea and green tea bioactive compounds may be beneficial in mitigating bone loss of this population and decreasing their risk of osteoporotic fractures. This review describes the effect of green tea or its bioactive components on bone health, with an emphasis on (i) the prevalence and etiology of osteoporosis; (ii) the role of oxidative stress and antioxidants in osteoporosis; (iii) green tea composition and bioavailability; (iv) the effects of green tea and its active components on osteogenesis, osteoblastogenesis, and osteoclastogenesis from human epidemiological, animal, as well as cell culture studies; (v) possible mechanisms explaining the osteoprotective effects of green tea bioactive compounds; (vi) other bioactive components in tea that benefit bone health; and (vii) a summary and future direction of green tea and bone health research and the translational aspects. In general, tea and its bioactive components might decrease the risk of fracture by improving bone mineral density and supporting osteoblastic activities while suppressing osteoclastic activities.

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Author: Masoumeh Akhlaghi and Brian Bandy

Green tea catechins are dietary antioxidant compounds that have been shown to protect against myocardial ischemia-reperfusion (IR) injury. Considering reports that catechins can induce phase 2 enzymes in cultured cells and some organs, we hypothesized that part of the protection to heart against IR injury may involve elevation of phase 2 enzyme activities. Rats were fed for 10 days with either control diet (sham and control groups) or the diet mixed with 0.25% green tea extract. At the end of 10 days, hearts were excised and subjected to global ischemia for 20 min followed by reperfusion for 2 hours. The hearts were compared for indices of cell death, oxidative stress, and phase 2 enzyme activities. Hearts from the green tea group had a 65% to 85% decrease in markers of apoptosis, a tendency to higher total glutathione, and higher activities of the phase 2 enzymes glutamate cysteine ligase and quinone reductase. The results support a possible involvement of phase 2 enzymes in the protection by green tea catechins against myocardial IR injury.

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Author: Rashmi Singh and Nahid Akhtar and Tariq M. Haqqi

A number of factors including inflammation and oxidative stress are believed to play a role in the development of chronic joint diseases. Green tea has become a popular drink and is consumed throughout the world. Extracts of green tea and polyphenols present therein have been shown to inhibit the inflammatory responses in vitro in different cell types and the development of arthritis in animal model studies. There is considerable evidence that (−)-epigallocatechin-3-gallate (EGCG), the predominant green tea polyphenol which mimic its effects, inhibits enzyme activities and signal transduction pathways that play important roles in inflammation and joint destruction in arthritis. After oral consumption EGCG become bioavailable and proteomic studies suggest that EGCG may directly interact with a large set of protein targets and alter the physiological response of the cells. Taken together these and other studies identify and support the use of EGCG as a possible chemopreventive agent with a potential to inhibit the development of arthritis. Here we review the biological effects of EGCG in an attempt to understand its pivotal molecular targets that directly affect the inflammation and joint destruction process for prevention and/or for the development of new therapeutics for arthritis in humans.

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Author: Joshua D. Lambert and Ryan J. Elias

Green tea (Camellia sinensis) is rich in catechins, of which (−)-epigallocatechin-3-gallate (EGCG) is the most abundant. Studies in animal models of carcinogenesis have shown that green tea and EGCG can inhibit tumorigenesis during the initiation, promotion and progression stages. Many potential mechanisms have been proposed including both antioxidant and pro-oxidant effects, but questions remain regarding the relevance of these mechanisms to cancer prevention. In the present review, we will discuss the redox chemistry of the tea catechins and the current literature on the antioxidant and pro-oxidative effects of the green tea polyphenols as they relate to cancer prevention. We report that although the catechins are chemical antioxidants which can quench free radical species and chelate transition metals, there is evidence that some of the effects of these compounds may be related to induction of oxidative stress. Such pro-oxidant effects appear to be responsible for the induction of apoptosis in tumor cells. These pro-oxidant effects may also induce endogenous antioxidant systems in normal tissues that offer protection against carcinogenic insult. This review is meant point out understudied areas and stimulate research on the topic with the hope that insights into the mechanisms of cancer preventive activity of tea polyphenols will result.

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Author: Marco Assunção and Maria J. Santos-Marques and Félix Carvalho and José P. Andrade

Author: Yan Xu and Jun-jian Zhang and Li Xiong and Lei Zhang and Dong Sun and Hui Liu

Responses to oxidative stress contribute to damage caused by chronic cerebral hypoperfusion, which is characteristic of certain neurodegenerative diseases. We used a rat model of chronic cerebral hypoperfusion to determine whether green tea polyphenols, which are potent antioxidants and free radical scavengers, can reduce vascular cognitive impairment and to investigate their underlying mechanisms of action. Different doses of green tea polyphenols were administered orally to model rats from 4 to 8 weeks after experimentally induced cerebral hypoperfusion, and spatial learning and memory were assessed using the Morris water maze. Following behavioral testing, oxygen free radical levels and antioxidative capability in the cortex and hippocampus were measured biochemically. The levels of lipid peroxidation and oxidative DNA damage were assessed by immunohistochemical staining for 4-hydroxynonenal and 8-hydroxy-2′-deoxyguanosine, respectively. Rats that received green tea polyphenols 400 mg/kg per day had better spatial learning and memory than saline-treated rats. Green tea polyphenols 400 mg/kg per day were found to scavenge oxygen free radicals, enhance antioxidant potential, decrease lipid peroxide production and reduce oxidative DNA damage. However, green tea polyphenols 100 mg/kg per day had no significant effects, particularly in the cortex. This study suggests that green tea polyphenols 400 mg/kg per day improve spatial cognitive abilities following chronic cerebral hypoperfusion and that these effects may be related to the antioxidant effects of these compounds.

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Author: Lei Li and C.-Y. Oliver Chen and Giancarlo Aldini and Elizabeth J. Johnson and Helen Rasmussen and Yasukazu Yoshida and Etsuo Niki and Jeffrey B. Blumberg and Robert M. Russell and Kyung-Jin Yeum

Epigallocatechin gallate, a major component of green tea polyphenols, protects against the oxidation of fat-soluble antioxidants including lutein. The current study determined the effect of a relatively high but a dietary achievable dose of lutein or lutein plus green tea extract on antioxidant status. Healthy subjects (50–70 years) were randomly assigned to one of two groups (n=20 in each group): (1) a lutein (12 mg/day) supplemented group or (2) a lutein (12 mg/day) plus green tea extract (200 mg/day) supplemented group. After 2 weeks of run-in period consuming less than two servings of lightly colored fruits and vegetables in their diet, each group was treated for 112 days while on their customary regular diets. Plasma carotenoids including lutein, tocopherols, flavanols and ascorbic acid were analyzed by HPLC-UVD and HPLC-electrochemical detector systems; total antioxidant capacity by fluorometry; lipid peroxidation by malondialdehyde using a HPLC system with a fluorescent detector and by total hydroxyoctadecadienoic acids using a GC/MS. Plasma lutein, total carotenoids and ascorbic acid concentrations of subjects in either the lutein group or the lutein plus green tea extract group were significantly increased (P<.05) at 4 weeks and throughout the 16-week study period. However, no significant changes from baseline in any biomarker of overall antioxidant activity or lipid peroxidation of the subjects were seen in either group. Our results indicate that an increase of antioxidant concentrations within a range that could readily be achieved in a healthful diet does not affect in vivo antioxidant status in normal healthy subjects when sufficient amounts of antioxidants already exist.

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Author: Qiong Li and Haifeng Zhao and Ming Zhao and Zhaofeng Zhang and Yong Li

As the organism ages, production of reactive oxygen species (ROS) increases while antioxidants defense capability declines, leading to oxidative stress in critical cellular components, which further enhances ROS production. In the brain, this vicious cycle is more severe as brain is particularly vulnerable to oxidative damage. In our study, 14-month-old female C57BL/6J mice were orally administered 0.05% green tea catechins (GTC, w/v) in drinking water for 6 months. We found that GTC supplementation prevented the decrease in total superoxide dismutase and glutathione peroxidase activities in serum as well as reduced the thiobarbituric acid reactive substances and protein carbonyl contents in the hippocampus of aged mice. The activation of transcriptional factor nuclear factor-kappa B and lipofuscin formation in pyramidal cells of hippocampal CA1 region, which are all related to oxidative stress, was also reduced after GTC treatment. We also found that long-term GTC treatment prevented age-related reductions of two representative post-synaptic proteins post-synaptic density 95 and N-methyl-d-aspartate receptor 1 in the hippocampus. These results demonstrated that chronic 0.05% green tea catechins administration may prevent oxidative stress related brain aging in female C57BL/6J mice.

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Author: Shigeki Yanagi and Kazuaki Matsumura and Akira Marui and Manabu Morishima and Suong-Hyu Hyon and Tadashi Ikeda and Ryuzo Sakata

Objective Ischemia–reperfusion injury is among the most serious problems in cardiac surgery. Epigallocatechin-3-gallate, a major polyphenolic component of green tea, is thought to be cardioprotective through its antioxidant activities. We investigated cardioprotective effects of oral epigallocatechin-3-gallate pretreatment against ischemia–reperfusion injury in isolated rat hearts and considered possible underlying mechanisms. Methods Rats were given epigallocatechin-3-gallate solution orally at 0.1, 1, or 10 mmol/L (n = 12 per group) for 2 weeks; controls (n = 12) received tap water alone for 2 weeks. Subsequently, Langendorff-perfused hearts were subjected to global ischemia for 30 minutes, followed by 60 minutes of reperfusion. Results Recoveries at 60 minutes after reperfusion of left ventricular developed pressure and maximum positive and minimum negative first derivatives of left ventricular pressure were significantly higher in 1-mmol/L group than in 0.1-mmol/L (P < .0001), 10-mmol/L (P < .05), and control (P < .0001) groups. Oxidative stress after reperfusion, as reflected by 8-hydroxy-2′-deoxyguanosine index, was lower in 1-mmol/L group than in control (P < .01) and 0.1-mmol/L (P < .05) groups. Western blot analysis after reperfusion showed p38 activation and active caspase-3 expression to be lower in 1-mmol/L group than in control group (P < .05). Conclusions Oral pretreatment with epigallocatechin-3-gallate preserved cardiac function after ischemia–reperfusion, an effect that may involve its antioxidative, antiapoptotic properties, although a high dose did not lead to dramatic improvement in cardiac function. Oral epigallocatechin-3-gallate pretreatment may be a novel and simple cardioprotective method for preventing perioperative cardiac dysfunction in cardiac surgery.

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