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The aim of this study was to compare the indices of glutathione antioxidant system and oxidative damage level in resistance trained and untrained subjects and to assess the antioxidant action of -lipoic acid in trained men exposed to muscle-damaging exercise. Thirteen trained and twenty untrained men (NT) participated in the comparative study. Then trained men were randomly assigned to TCON group (control) or TALA group (-lipoic acid, 600 mg . day-1, for 8 days) and performed isometric/isokinetic effort of quadriceps muscles. The study has shown the significantly higher erythrocyte levels of glutathione (GSH), glutathione reductase (GR) and glutathione peroxidase (GPx) in TCON than NT but no differences in plasma lipid peroxidation (TBARS) and protein carbonylation (PC). However, total thiol (TT) concentration was two-fold lower in TCON than NT group. -Lipoic acid variously influenced the post-exercise levels of GSH (+40%), GR (-24%) and GPx (+29%), but markedly reduced by over 30% the resting and post-exercise TBARS and PC in TALA compared with TCON. TT concentration significantly increased in TALA but it did not reach the high level which was found in untrained group. It is concluded that -lipoic acid supplementation diminishes oxidative damage. It does not abolish differences in glutathione antioxidant system between untrained and trained subjects but modulates a pro-antioxidant response to the muscle-damaging exercise.
In both forms of muscular dystrophy, the severe Duchenne’s muscular dystrophy (DMD) with lifespan shortened to about 20 years and the milder Becker dystrophy (BDM) with normal lifespan, the gene defect is located at chromosome locus Xp21. The location is the same in the experimental model of DMD in the mdx mice. As the result of the gene defect a protein called dystrophin is either not synthesized, or is produced in traces. Although the structure of this protein is rather well established there are still many controversies about the dystrophin function. The most accepted suggestion supposes that it stabilizes sarcolemma in the course of the contraction-relaxation cycle. Solving the problem of dystrophin function is a prerequisite for introduction of an effective therapy. Among the different factors which might be responsible for the appearance and progress of dystrophic changes in muscles there is an excessive action of oxidative stress. In this review data indicating the influence of oxidative stress on the severity of the pathologic processes in dystrophy are discussed. Several pieces of data indicating the action of oxidative damage to different macromolecules in DMD/BDM are presented. Special attention is devoted to the degree of oxidative damage to muscle proteins, the activity of neuronal nitric oxide synthase (nNOS) and their involvement in defining the severity of the dystrophic processes. It is indicated that the severity of the morbid process is related to the degree of oxidative damage to muscle proteins and the decrease of the nNOS activity in muscles. Estimation of the degree of the destructive action of oxidative stress in muscular dystrophy may be a useful marker facilitating introduction of an effective antioxidant therapy and regulation of nNOS activity.
We have found that isoguanine (¡G) can pair with thymine (iG T) and the non- natural base, 5-methylisocytosine (iG x iCM) during template directed synthesis catalyzed by AMV reverse transcriptase. The ratio of these pairings is about 1:10, irrespectively which of the templates, poly(C,iG) or poly(I,iG) is used. This ratio corresponds to the ratio of 2-OH and 2-keto tautomers in monomer in aqueous sol ution and apparently it is not influenced by the template context. Our results indicate also that formation of the reverse transcriptase catalyzed base pairs between iG and A, G or C can occur only at a low frequency, comparable to the frequency, of mismatches of.
The amount of all bases, except for 5,6-dihydroxyuracil were significantly increased in rat DNA upon cobalt-60 y-irradiation. Control values were recovered 12 h after irradiation. The extent of DNA damage and repair was different for particular bases.
This study focuses on anti-glycemic and anti-hepatotoxic effects of mangosteen vinegar rind (MVR) on fi ve weeks high-fat diet (HFD) / single dose streptozotocin (STZ) 30 mg/kg BW induced male ICR diabetic mice. Mice were randomly divided into fi ve groups (n=6), normal control, diabetic control, and diabetic groups treated with MVR 100, 200 mg/kg BW and glibenclamide 60 mg/kg BW for one week. After the treatment, lipid profi le, glycogen and bilirubin contents, oxidative damage (malondialdehyde, MDA), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT) were measured in plasma and/or liver tissues. MVR and glibenclamide treatment to HFD/STZ-induced diabetic mice signifi cantly reduced their plasma glucose, plasma lipid profi le, and hepatic lipid profi le (P<0.05). Increased hepatic glycogen content indicates improvement of insulin sensitivity. Moreover, oxidative damage markers were ameliorated in MVR- and glibenclamide-treated groups compared to the diabetic control group. MVR with phenolic compounds content of 75 mg GAE/g dry weight and antioxidant potential of 303 mmol/L Trolox/g dry weight acted as a hepatoprotective agent against oxidative damage.
Hybrid cells derived from stem cells play an important role in organogenesis, tissue regeneration and cancer formation. However, the fate of hybrid cells and their range of function are poorly understood. Fusing stem cells and somatic cells induces somatic cell reprogramming, and the resulting hybrid cells are embryonic stem cell-like cells. Therefore, we hypothesize that fusion-induced hybrid cells may behave like ES cells in certain microenvironments. In this study, human hepatic cells were induced to apoptosis with H2O2, and then co-cultured with hybrid cells that had been derived from mouse ES cells and human hepatic cells using a transwell. After co-culturing, the degree of apoptosis was evaluated using Annexin-V/PI double-staining analysis, flow cytometry and Western-blot. We observed that H2O2-induced cell apoptosis was inhibited by co-culture. In addition, the activity of injury-related enzymes (GSH-Px, LDH and SOD) and the level of albumin release in the co-culture system trended toward the level of normal undamaged hepatic cells. The stably increased levels of secretion of ALB in the co-culture system also confirmed that co-culture with hybrid cells helped in recovery from injury. The fate of the hybrid cells was studied by analyzing their gene expression and protein expression profiles. The results of RT-PCR indicated that during co-culturing, like ES cells, hybrid cells differentiated into hepatic lineage cells. Hybrid cells transcripted genes from both parental cell genomes. Via immunocytochemical analysis, hepatic directional differentiation of the hybrid cells was also confirmed. After injecting the hybrid cells into the mouse liver, the GFP-labeled transplanted cells were distributed in the hepatic lobules and engrafted into the liver structure. This research expands the knowledge of fusion-related events and the possible function of hybrid cells. Moreover, it could indicate a new route of differentiation from pluripotent cells to tissue-specific cells via conditional co-culture.
In this study we investigated the level of 8-oxo-2'-deoxyguanosine (8-oxodG) in DNA of Cardamine pratensis plants subjected to different growth conditions trying to answer the question whether factors like light and water accessibility or low temperature may have an impact on the total DNA oxidative damage. The level of this modified nucleoside was determined using HPLC coupled to UV absorbance and electrochemical detection (HPLC-UV-EC). We did not observe any statistically significant differences in 8-oxodG level between DNA of etiolated and light exposed plants as well as between DNA of regularly watered and drought-subjected plants. In contrast, we have shown that chilling (1®C for 28 h) brings about the increase of 8-oxodG level in DNA.
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