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A review of literature dealing with the reaction of formaldehyde with aminoacids, peptides and proteins was done. The changes in these compounds' structures and functions resulting from formaldehyde binding were discussed.
Amifostine is one of the cytoprotective drugs used during anticancer therapy. Amifostine as a thiol compound possesses antioxidant properties and protects only healthy cells against damage, mainly by scavenging reactivity oxygen species, competing with oxygen to prevent oxygen radical interactions with DNA, and promoting cell repair through hydrogen donation to reactive oxygen species. The aim of the present study was to evaluate antioxidative ability of amifostine in blood serum of rats exposed to cyclophosphamide during two weeks after drug administration. We show that amifostine only to a small degree prevents disorganisation of antioxidant systems of blood serum of rats caused by cyclophosphamide action. It is probably connected with low concentrations of amifostine active metabolites in the serum.
Lipid peroxidation is a process involving the oxidation of polyunsaturated fatty acids (PUFAs), which are basic components of biological membranes. Reactive electrophilic compounds are formed during lipid peroxidation, mainly α,β-unsaturated aldehydes. These compounds yield a number of adducts with DNA. Among them, propeno and substituted propano adducts of deoxyguanosine with malondialdehyde (MDA), acrolein, crotonaldehyde and etheno adducts, resulting from the reactions of DNA bases with epoxy aldehydes, are a very important group of adducts. The epoxy aldehydes are more reactive towards DNA than the parent unsaturated aldehydes. The compounds resulting from lipid peroxidation mostly react with DNA showing both genotoxic and mutagenic action; among them, 4-hydroxynonenal is the most genotoxic, while MDA is the most mutagenic. DNA damage caused by the adducts of lipid peroxidation products with DNA can be removed by the repairing action of glycosylases. The formed adducts have been hitherto analyzed using the IPPA (Imunopurification-32P-postlabelling assay) method and via gas chromatography/electron capture negtive chemical ionization/mass spectrometry (GC/EC NCI/MS). A combination of liquid chromatography with electrospray tandem mass spectrometry (LC/ES-MSMS) with labelled inner standard has mainly been used in recent years.
Activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-R) and concentration of ascorbate, a-tocopherol, non-protein and protein-bound sulfhydryi compounds and thio- barbituric acid-reactive substances (TBA-rs) were measured in liver and serum of rats 6, 12 and 24 h and 2, 5 and 7 days after intoxication with 1.5 g or 3.0 g methanol/kg b.w. Liver GSH-Px and GSSG-R activities and SH-groups and ascorbate content were significantly diminished at 6 and 24 h, while TBA-rs were increased. Serum SOD, GSH-Px and GSSG-R activities and SH-groups concentration were reduced while TBA-rs were elevated. The changes were more intensive after application of the higher dose of methanol. It is concluded that methanol impairs the liver and blood serum antioxidant mechanisms in rats.
Changes in the composition and physicochemical properties of liver cell membranes appearing as the result of ethanol intoxication and the aging process are mainly due to reactive oxygen species (ROS). The destructive action of free radicals can be neutralized by administering antioxidants, especially natural ones like green tea. For this reason, the purpose of this study was to estimate the efficacy of green tea’s influence on the physicochemical and biochemical properties of the rat liver as affected by the aging process and/or chronic ethanol intoxication. Several methods were used to evaluate this effect. Qualitative and quantitative composition of phospholipids in the membrane was determined by High Performance Liquid Chromatography (HPLC). The electrophoresis technique was used to determine the surface charge density of the rat liver cell membrane. The process of aging causes a decrease in the total amount of phospholipids, increases lipid peroxidation products and surface charge density of liver cell membrane. The results also demonstrate that ethanol administration provoked increase phospholipid composition, lipid peroxidation products and surface charge density in liver cell membrane. The ingestion of green tea with ethanol partially prevented these ethanol-induced and/or aging changes. Moreover, long-term drinking of green tea partially prevents changes in structure and function of membrane phospholipids caused by chronic ethanol intoxication.
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