PURPOSE:Green tea due to its content of catechins reveals strong antioxidative activity, which is manifested among others by its ability to inhibit free radical generation, scavenge free radicals as well as chelate transition metal ions that catalyse free radical reactions. The influence of green tea extract, epicatechin (EC), epicatechin galate (ECG) as well as epigallocatechin galate (EGCG) on oxidative modifications of LDL of human blood serum has been examined in the present study.MATERIALS AND METHODS:This influence has been evaluated by measurement of the concentration of first products of lipid peroxidation--conjugated dienes and lipid hydroperoxides as well as by determining tryptophan and dityrosine content-- the markers of protein oxidative modification.RESULTS:Catechins and green tea abilities to protect lipophilic antioxidant--alpha-tocopherol against oxidation have been also examined. The results reveal that peroxidation of LDL is markedly prevented by green tea extract and in a slightly weaker way by catechins (EGCG in particular), which is manifested by a decrease in concentration of conjugated dienes, lipid hydroperoxides, MDA, dityrosine and by an increase in tryptophan content. Both green tea as well as catechins (EGCG in particular) have been also revealed to prevent decrease in concentration of alpha-tocopherol in oxidating conditions.CONCLUSIONS:It can be assumed that green tea and to a lesser degree catechins, protecting the basic antioxidant of LDL-alpha-tocopherol, prevent oxidative modification of LDL.

It is known that aging is characterized by changes in cell metabolism resulting in modification of the structure and function of cell membrane components which is mainly the consequence of reactive oxygen species action. These disturbances are also enhanced by different xenobiotics, e.g. ethanol. Therefore, the aim of this paper is to examine green tea influence on total antioxidant status (TAS) and on composition and electric charge of erythrocyte membrane phospholipids in ethanol intoxicated rats of various ages. Antioxidant abilities of erythrocytes were estimated by measuring TAS. Qualitative and quantitative composition of phospholipids in the membrane was determined by HPLC, while the extent of erythrocytes lipid peroxidation was estimated by HPLC measurement of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) levels. Electrophoresis was used to determine the surface charge density of the rat erythrocyte membrane. It was shown that the process of aging was accompanied by a decrease in TAS and in the total amount of phospholipids as well as by enhancement of lipid peroxidation and increase in surface charge density of erythrocyte membrane. Ethanol administration caused, in term, decrease in TAS and increase in the level of all phospholipids and lipid peroxidation products. Ethanol as well significantly enhanced changes in surface charge density of erythrocyte membrane. The ingestion of green tea partially prevented decrease in erythrocyte antioxidant abilities observed during aging and ethanol intoxication. Moreover, long-term drinking of green tea protects the structure of the erythrocytes membrane disturbed during aging process and/or chronic ethanol intoxication.

Methanol is oxidized into the formaldehyde and formate and these processes are accompanied by free radicals' generation. Formaldehyde and free radicals induce chemical modifications of proteins, leading to changes in their structure and function. The aim of this paper has been to evaluate the effect of N-acetylcysteine and vitamin E derivative U83836E on free radicals' generation and protein modifications induced during acute methanol intoxication. U83836E is an analog of alpha-tocopherol and similarly protects cells against oxidative damage. Moreover, this compound has hydrophilic properties and can be dissolved in an aqueous phase of blood and interstitial fluid, and next, membranes readily take it up. This compound belonging to the benzopyran family contains the reactive trolox ring and possesses antioxidant properties. The ESR determination indicates the increase in free radicals' signal 6 and 12 h after intoxication. Methanol ingestion causes a significant decrease in GSH level (by about 35%) and a significant increase in the lipid peroxidation product malondialdehyde (by about 25%). During methanol metabolism the aromatic amino acids of proteins are modified-the amount of carbonyl groups is increased (by about 42%) and fluorescence intensity of tryptophan is statistically decreased (by about 30%). The increase (by about 200%) in bityrosine fluorescence is also observed. Moreover, a significant decrease in free sulphydryl (by about 40%) and amino groups (by about 30%) in liver proteins is observed during intoxication. This is accompanied by the loss of lysosomal protease-cathepsin B activity (by about 25%). N-acetylcysteine (in dose 150 mg/kg body weight) and U83836E (in dose 10 mg/kg body weight) prevent free radicals' generation to a similar degree. U83836E protects membrane phospholipids against peroxidation a little stronger than N-acetylcysteine (concentration of MDA is decreased by 9 to 20% in the U83836 group and by 7 to 14% in the N-acetylcysteine group compared to methanol group). However after treating methanol-intoxicated rats with N-acetylcysteine, the changes in protein modification parameters are significantly smaller than in the group receiving methanol alone and they are a little smaller than after U83836E application. These findings suggest that N-acetylcysteine and to a smaller degree U83836E protect protein from modification in methanol intoxication, which can prevent liver pathologies.

Ethanol metabolism is accompanied by generation of free radicals, which stimulates lipid peroxidation. Natural antioxidants are particularly useful in such a situation. The current study was designed to investigate the efficacy of green tea, as a source of water-soluble antioxidants (catechins), on lipid peroxidation in liver, brain, and blood induced by chronic (4 weeks) ethanol intoxication in rats. Feeding of ethanol led to a significant increase in lipid peroxidation, as measured by increased concentrations of lipid hydroperoxides, 4-hydroxynonenal, and malondialdehyde. Feeding of ethanol also changed the glutathione-dependent lipid hydroperoxide decomposition system, resulting in a decrease in both reduced glutathione concentration and activity of glutathione peroxidase. Observed changes were statistically significant in all examined tissues. Enhancement in lipid peroxidation was associated with disruption of hepatocyte cell membranes, as observed through electron microscopic evaluation. Green tea protects phospholipids from enhanced peroxidation and prevents changes in biochemical parameters and morphologic changes observed after ethanol consumption. These results support the suggestion that green tea protects membranes from peroxidation of lipids associated with ethanol consumption.

Ethanol oxidation to acetaldehyde and next to acetate is accompanied by free radical generation. Free radicals can affect cell integrity when antioxidant mechanisms are no longer able to cope with the free radical generation observed in ethanol intoxication. Natural antioxidants are particularly useful in such a situation. The present study was designed to investigate the efficacy of green tea as a source of water-soluble antioxidants (catechins) on the liver and blood serum antioxidative potential of rats chronically (28 days) intoxicated with ethanol. Alcohol caused a decrease in liver superoxide dismutase, glutathione peroxidase and catalase activities and an increase in activity of glutathione reductase. Moreover, a decrease in the level of reduced glutathione, ascorbic acid, vitamins A and E and beta-carotene were observed. The activity of serum glutathione peroxidase decreased while glutathione reductase activity increased. The level of serum non-enzymatic antioxidants was also decreased in the liver. Alcohol administration caused an increase in the liver and serum lipid peroxidation products, measured as thiobarbituric acid-reactive substances. However, green tea prevents the changes observed after ethanol intoxication. Green tea also protects membrane phospholipids from enhanced peroxidation. These results indicate a beneficial effect of green tea in alcohol intoxication.

This paper reports data on the effect of green tea on the lipid peroxidation products formation and parameters of antioxidative system of the liver, blood serum and central nervous tissue of healthy young rats drinking green tea for five weeks. The rats were permitted free access to solubilized extract of green tea. Bioactive ingredients of green tea extract caused in the liver an increase in the activity of glutathione peroxidase and glutathione reductase and in the content of reduced glutathione as well as marked decrease in lipid hydroperoxides (LOOH), 4-hydroksynonenal (4-HNE) and malondialdehyde (MDA). The concentration of vitamin A increased by about 40%. Minor changes in the measured parameters were observed in the blood serum. GSH content increased slightly, whereas the index of the total antioxidant status increased significantly. In contrast, the lipid peroxidation products, particularly MDA was significantly diminished. In the central nervous tissue the activity of superoxide dismutase and glutathione peroxidase decreased while the activity od glutathione reductase and catalase increased after drinking green tea. Moreover the level of LOOH, 4-HNE and MDA significantly decreased. The use of green tea extract appeared to be beneficial to rats in reducing lipid peroxidation products. These results support and substantiate traditional consumption of green tea as protection against lipid peroxidation in the liver, blood serum, and central nervous tissue.

Background: The free radical theory of aging suggested that aging is caused by changes in the redox state and by an increase in oxidative damage of cell components. Aims: The effect of green tea on the antioxidative system and lipid and protein peroxidation in the liver of aged rats were examined. Methods: 2- and 12-months old male Wistar rats received green tea solution (3g/11) for 4 weeks and in the liver homogenates the level of antioxidants and lipid and protein oxidation markers was determined. Results: In the liver of 2- and 12-months rats, drinking green tea caused increase in the activity of Cu,Zn-SOD, GSH-Px and GSSG-R. Activity of CAT was increased in young rats and decreased in older. The level of GSH, vitamin E and TAS was increased in both age groups, while vitamin C level was decreased in the liver of 2-months rats. Green tea significantly decreased level of malondialdehyde and carbonyl groups. Conclusion: Green tea partially protects cell compounds against modifications observed during aging.