Protective effects of green tea on intestinal ischemia-reperfusion injury.

OBJECTIVE: The intestinal mucosa is known to be adversely affected by ischemia-reperfusion (I/R). Previously we showed that green tea protects the intestinal mucosa from fasting-induced damage. The aim of this study is to determine whether green tea has any protective role in I/R of the intestine. METHODS: Three groups of male rats were used in this study. Group I (I/R) underwent I/R of the intestine (30 min of ischemia followed by 1 h of reperfusion). Group II (green tea + I/R) was given green tea for 2 wk before inducing I/R. Group III (control) had sham I/R. After the experiments, the jejunum was removed and the tissues were processed for histopathologic examination and immunohistochemical analysis for cell proliferation markers and antioxidant enzymes. RESULTS: The intestinal mucosa in group II was preserved compared with that in group I. The expressions of cellular proliferation markers (proliferating cell nuclear antigen and Ki-67) and cellular antioxidants (superoxide dismutase and catalase) in group II were similar to those in group III and much less than in group I, reflecting the protective effects of green tea in group II animals. CONCLUSION: In this animal model, administration of green tea before inducing I/R protects the intestinal mucosa from injury.

Fasting-induced intestinal damage is mediated by oxidative and inflammatory responses.

BACKGROUND: Green tea has been shown to repair fasting-induced mucosal damage in rat intestine. The aim of this study was to elucidate the underlying mechanism. METHODS: Five groups of rats were used. Group 1 had free access to chow diet and water, and those in group 2 were fasted for 3 days. Animals in group 3 were fasted for 3 days, then were allowed drinking water for a further 7 days. Groups 4 and 5 were fasted for 3 days, then given drinking water containing green tea or vitamin E respectively for 7 days. Blood was collected for estimation of total plasma antioxidants, and jejunal samples were used for immunohistochemical analysis of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx), and for estimation of myeloperoxidase (MPO) activity. RESULTS: Use of green tea was associated with a significant increase in total plasma antioxidants (P < 0.001), and mucosal SOD (P < 0.001), catalase (P = 0.006) and GPx (P = 0.017), but a significant decrease in MPO activity (P < 0.001). Vitamin E produced similar changes, but the effects were smaller. CONCLUSION: Green tea reverses the fasting-induced damage to the intestinal mucosa by its antioxidant and anti-inflammatory effect.

Indications of the mechanisms involved in improved sperm parameters by zinc therapy.

OBJECTIVE: To determine possible indications of the mechanisms involved in improved sperm parameters by zinc therapy in asthenozoospermic men. SUBJECTS AND METHODS: Forty-five men with asthenozoospermia (>or=40% immotile sperm) were randomized into four therapy groups: zinc only: n = 11; zinc + vitamin E: n = 12 and zinc + vitamins E + C: n = 14 for 3 months, and non-therapy control group: n = 8. Semen analysis was done according to WHO guidelines. Malone dialdehyde, tumour necrosis factor-alpha (TNF-alpha), total antioxidant capacity, superoxide dismutase (SOD) and glutathione peroxidase were determined in the semen and serum. Antisperm antibodies IgG, IgM and IgA were evaluated by immunobeads. Sperm chromatin integrity was determined by acid denaturation by acridine orange and sperm apoptosis by light and electron microscopy. The effect of zinc on in vitro induced sperm oxidative stress by NADH was evaluated. RESULTS: Asthenozoospermia was significantly associated with oxidative stress with higher seminal malone dialdehyde (8.8 vs. 1.8 mmol/l, p < 0.001) and TNF-alpha (60 vs. 12 pg/l, p < 0.001), and low total antioxidant capacity (1.8 vs. 8.4, p < 0.01), SOD (0.8 vs. 3.1, p < 0.01) and glutathione peroxidase (1.6 vs. 4.2, p < 0.05), compared to normozoospermia. Zinc therapy alone, in combination with vitamin E or with vitamin E + C were associated with comparably improved sperm parameters with less oxidative stress, sperm apoptosis and sperm DNA fragmentation index (DFI). On the whole, there was no difference in the outcome measures between zinc only and zinc with vitamin E and combination of vitamins E + C. In the in vitro experiment zinc supplementation resulted in significantly lower DFI (14-29%, p < 0.05) compared to zinc deficiency. CONCLUSION: Zinc therapy reduces asthenozoospermia through several mechanisms such as prevention of oxidative stress, apoptosis and sperm DNA fragmentation.

Brain selenium accumulation in rat pups of selenium supplemented mothers.

Selenium is essential for normal mammalian development. Being a component of antioxidant enzyme, glutathione peroxidase, it plays a major role in protecting the cells from free radical damage. The level of glutathione peroxidase was directly related to the amount of selenium present in various tissues and organs. A decrease in selenium leads to various pathological changes in humans as well as in various laboratory animals. The aim of the present study was to understand whether there is an increase in the level of selenium in different brain regions of rat pups whose mothers were supplemented with selenium, either 2 or 4 mg/l of their drinking water throughout the period of their pregnancy. There was a significant increase in the level of selenium in the cerebellum, cortex and hypothalamic and hippocampal tissues of selenium supplemented mothers as compared with those of non-supplemented mothers. The brain stem of these animals did not show any significant difference in the level of selenium. Furthermore, the differences in the level of selenium between the rat pups of 2 mg/l selenium supplemented mothers and 4 mg/l selenium supplemented mothers were not statistically significant. These studies suggest that supplementation of selenium to mothers during the period of their pregnancy can selectively increase the level of this trace element in different brain regions. Further studies are necessary to understand the significance of selective accumulation of selenium in specific brain regions on brain development and function.

Pre- and postnatal tissue selenium of the rat in the growing state.

The aim of this study is to quantify the selenium (Se) content (in microg/g) during different gestational periods in rat fetal tissues, and to follow up the changes in the Se content of the placenta, fetal head, liver and lung during gestation and postpartum periods. Locally reared virgin female Wistar rats were mated. Pregnant rats were sacrificed on days 15, 18 and 21 of pregnancy. Newborn pups at the age of 3 days and rats at the age of 1 month were also investigated. There was a gradual increase in placental and whole head Se content as gestation proceeded compared to day 15; however, the differences between the groups were not statistically significant. The liver Se content at day 18 of gestation was significantly higher than at day 21 of gestation and in rats at 3 days of age, but lower than the Se content of the liver of rats at the age of 1 month and the differences were statistically significant. The lung Se content was higher at day 18 of gestation than at day 21 and in the 3-day-old rats, and all differences between all groups were statistically significant except when the lung Se content at day 18 is compared to that of 1-month-old animals. The continuous increase in the Se content of the placental tissues and the whole head, although not significant statistically, may indicate that the fetus relies heavily on its supply of Se from the maternal blood and in part on the supply of thyroid hormones which are important for brain development, as evidence exists that T(4) and T(3) are present in the fetal brain in early fetal life before the onset of fetal thyroid function. The higher content of Se on day 18 and its decline on day 21 of gestation in the liver may imply that it is stored and being utilized partly in other tissues for other functions and particularly for thyroid hormone synthesis, metabolism and functions.

Selenium and liver cirrhosis.

Effects of selenium deficiency, induced by thioacetamide, were investigated in rats. Thioacetamide (0.3 g/L) given in drinking water, as expected, caused a significant loss of selenium from the liver. It was accompanied by liver cirrhosis and a significant increase in the liver weight as well as liver to body weight ratio. A significant loss of selenium from spleen was also accompanied by an increase in its weight. Weights of lungs, testis and kidney, however, were not affected by thioacetamide and there was no change in their selenium content. Plasma levels of selenium were significantly reduced in the thioacetamide treated group. All these changes were confirmed to be due to selenium deficiency caused by thioacetamide, as supplementation with selenium reversed these changes. The mode of action of selenium is unknown but may involve anti-oxidant defense mechanisms.