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ABSTRACT: Methylglyoxal (MG) is a reactive dicarbonyl compound that is produced endogenously from glycolytic intermediates and via gluconeogenesis. Elevated MG levels in diabetes patients are believed to cause diabetic complications. MG-induced crosslinking products from the covalent binding of DNA or protein alone or together could be relevant to carcinogenesis and multiple complications in diabetes. However, the mechanisms governing DNA crosslink formation by MG are unclear. We investigated whether MG could induce DNA crosslinks in human ECV304 cells and the possible mechanism of this action. The level of DNA crosslinks and reactive oxygen species production were assayed by a modified alkaline Comet assay and a 2',7' dichlorofluorescin diacetate (DCHF-DA) assay, respectively. MG caused a time- and dose-dependent increase in DNA crosslinks and a dose-dependent increase in protein carbonylation in ECV304 cells. Addition of 2 mM MG resulted in a transient increase in protein carbonylation, and this increase peaked within 2 h and then rapidly decreased. Most notably, MG did not cause significantly enhanced ROS generation in ECV304 cells. Co-treatment with carbonyl-scavenging drugs, such as aminoguanidine, N-acetyl-L-cysteine, and glutathione, significantly inhibited the formation of DNA crosslinks by MG, whereas co-treatment with the antioxidant ascorbic acid did not. In conclusion, our results imply that MG induces DNA crosslink formation in ECV304 cells via a reactive oxygen species-independent protein carbonylation pathway. Our findings also suggest that non-toxic aminothiol antioxidants with carbonyl scavenging capabilities are potential therapeutic agent for MG-related diseases, such as diabetes and neurodegeneration. Furthermore, our findings also imply that DNA nonbinding proteins, bovine serum albumin might be able to crosslink calf thymus DNA in the presence of MG.
Toxicology in Vitro 02/2013; · 2.78 Impact Factor
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ABSTRACT: Chrysin, apigenin, and luteolin are flavones that differ in their number of hydroxyl groups in the B ring. In this study, we investigated the protection by chrysin, apigenin, and luteolin against tert-butyl hydroperoxide (tBHP)-induced oxidative stress and the possible mechanisms involved in rat primary hepatocytes. Chrysin, apigenin, and luteolin dose-dependently up-regulated the protein expression of heme oxygenase 1 (HO-1) and glutamate cysteine ligase (GCL) catalytic (GCLC) and modifier subunit (GCLM) and increased the intracellular glutathione (GSH) content and the ratio of GSH to oxidized GSH. Among the flavones studied, chrysin showed the greatest induction of HO-1, GCLC, and GCLM protein expression and GSH content. Cellular reactive oxygen species production induced by tBHP was attenuated by pretreatment with chrysin, apigenin, and luteolin (P < .05), and this protection was reversed by the GCL inhibitor l-buthionine-S-sulfoximine and the HO-1 inhibitor zinc protoporphyrin. Chrysin, apigenin, and luteolin activated extracellular signal-regulated protein kinase 2 (ERK2), nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation, nuclear Nrf2-antioxidant responsive element (ARE) binding activity, and ARE-dependent luciferase activity. Both ERK2 and Nrf2 siRNAs attenuated chrysin-induced HO-1, GCLC, and GCLM protein expression. Taken together, these results suggest that chrysin, apigenin, and luteolin inhibit tBHP-induced oxidative stress by up-regulating HO-1, GCLC, and GCLM gene transcription via the ERK2/Nrf2/ARE signaling pathways in rat primary hepatocytes.
Archive für Toxikologie 08/2012; · 4.67 Impact Factor
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ABSTRACT: Butachlor is the most commonly used herbicide on paddy fields in Taiwan and throughout Southeast Asia. Since paddy fields provide habitat for pond breeding amphibians, we examined growth, development, time to metamorphosis, and survival of alpine cricket frog tadpoles (Fejervarya limnocharis) exposed to environmentally realistic concentrations of butachlor. We documented negative impacts of butachlor on survival, development, and time to metamorphosis, but not on tadpole growth. The 96 h LC(50) for tadpoles was 0.87 mg/l, much lower than the 4.8 mg/l recommended dosage for application to paddy fields. Even given the rapid breakdown of butachlor, tadpoles would be exposed to concentrations in excess of their 96 h LC(50) for an estimated 126 h. We also documented DNA damage (genotoxicity) in tadpoles exposed to butachlor at concentrations an order of magnitude less than the 4.8 mg/l recommended application rate. We did not find that butachlor depressed cholinesterase activity of tadpoles, unlike most organophosphorus insecticides. We conclude that butachlor is likely to have widespread negative impacts on amphibians occupying paddy fields with traditional herbicide application.
Ecotoxicology 03/2011; 20(2):377-84. · 2.36 Impact Factor
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ABSTRACT: Andrographolide is the most abundant diterpene lactone in Andrographis paniculata, which is widely used as a traditional medicine in Southeast Asia. Heme oxygenase 1 (HO-1) is an antioxidant enzyme encoded by a stress-responsive gene. HO-1 has been reported to inhibit the expression of adhesion molecules in vascular endothelial cells (EC). Intercellular adhesion molecule (ICAM-1) is an inflammatory biomarker that is involved in the adhesion of monocytes to EC. In this study, we investigated the effect of andrographolide on the expression of ICAM-1 induced by tumor necrosis factor alpha (TNF-alpha) in EA.hy926 cells and the possible mechanisms involved. Andrographolide (2.5-7.5 microM) inhibited the TNF-alpha-induced expression of ICAM-1 in a dose-dependent manner and resulted in a decrease in HL-60 cell adhesion to EA.hy926 cells (p < 0.05). In parallel, andrographolide significantly induced the expression of HO-1 in a concentration-dependent fashion (p < 0.05). Andrographolide increased the rate of nuclear translocation of nuclear factor erythroid 2-related 2 (Nrf2) and induced antioxidant response element-luciferase reporter activity. Transfection with HO-1-specific small interfering RNA knocked down HO-1 expression, and the inhibition of expression of ICAM-1 by andrographolide was significantly reversed. These results suggest that stimulation of Nrf2-dependent HO-1 expression is involved in the suppression of TNF-alpha-induced ICAM-1 expression exerted by andrographolide.
Journal of Agricultural and Food Chemistry 07/2010; 58(13):7641-8. · 2.82 Impact Factor
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ABSTRACT: Epidemiologic studies have demonstrated that chronic arsenic exposure is associated with the incidence of chronic diseases. This association is partly related to the increase in reactive oxygen species (ROS) overload and protein oxidation that result from arsenic exposure. In this study, we intended to identify proteins susceptible to oxidative carbonylation by sodium arsenite and the impact of carbonylation on the function of these proteins in human umbilical vein endothelial cells (HUVECs). The 2,4-dinitrophenylhydrazine (DNPH) dot-blot assay revealed that arsenite (0-50 μM) dose-dependently increased protein carbonylation. Consistent with these findings, the cellular ROS level as measured by 2',7'-dichlorofluorescein diacetate (DCHF-DA) assay was increased in cells exposed to arsenite. By two-dimensional gel electrophoresis and matrix assist laser desorption ionization time of flight mass spectrometry (MALDI-TOF/MS), one glycolytic enzyme, enolase-α, two cytoskeleton proteins, fascin (F-actin associated protein) and vimentin, and two protein quality control proteins, HSC70 (heat-shock cognate protein 70), and PDIA3 (protein disulfide isomerase family A, member 3) were identified to be arsenic-sensitive carbonlyated proteins. Accompanied by carbonylation, enolase-α activity was dose-dependently decreased and the F-actin filament network was disturbed. Taken together, our results suggest that arsenite exposure results in the generation of carbonylated proteins, and the resultant changes in energy metabolism and in the cytoskeletal network may partly lead to cell damage.
Environmental Toxicology 03/2010; 26(5):459-71. · 2.41 Impact Factor
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ABSTRACT: Monascus sp. fermented products are known for their antihypercholesterolemic effects; however, their antioxidant and anti-inflammatory activities are different from those of many plant-derived foods. To evaluate the effect of turmeric addition into the medium on the antioxidant and anti-inflammatory activities of Monascus pilosus fermented products, we cultured uninoculated PDB medium (PDB), inoculated PDB medium (MP), uninoculated turmeric-containing PDB medium (PDBT), and inoculated turmeric-containing PDB medium (MPT). The broth and mycelia were collected, freeze-dried, and extracted to evaluate their free radical scavenging and iron-chelating activities, inhibition of peroxidation, phenolic and curcuminoid contents, and cellular antioxidant activity. The effects of the extracts on cell viability, cytokines and nitric oxide (NO) production, and expression of enzymes that regulate antioxidation and inflammation were also evaluated. The results showed that MPT had a significantly higher antioxidant activity than PDB, MP, and PDBT at all fermentation time points; moreover, the fermentation process significantly increased the phenolic and curcuminoid contents of MPT. As compared with MP, MPT had a more significant effect on down-regulating the production of NO and TNF-alpha as well as the expression of inducible nitric oxide synthase, cyclooxygenase-2, glutathione peroxidase, superoxidase dismutase, and catalase. After the inherent levels of antioxidant and anti-inflammatory capacities were increased, the modified M. pilosus fermented product demonstrated a higher antiatherosclerotic value than the unmodified product.
Journal of Agricultural and Food Chemistry 11/2009; 57(23):11397-405. · 2.82 Impact Factor
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ABSTRACT: Cigarette smoke is a mixture of chemicals that cause direct or indirect oxidative stress in different cell lines. We investigated the effect of nonfractionated cigarette smoke extract (CSE) on protein carbonylation in human THP-1 cells. Cells were exposed to various concentrations (2.5-20%) of CSE for 30 min, and protein carbonylation was assessed by use of the sensitive 2,4-dinitrophenylhydrazine immuno-dot blot assay. CSE-induced protein carbonylation exhibited a dose-response relation with CSE concentrations. However, with prolonged exposure to CSE, significant decrements were observed when compared with the 30 min exposure. Cotreatment of THP-1 cells with antioxidants (N-acetyl-cysteine, S-allyl-cysteine, and alpha-tocopherol) and copper(II) ion chelators (d-penicillamine) during CSE exposure significantly reduced protein carbonylation, whereas cotreatment with antioxidants (vitamin C and trolox) and a metal chelator (EDTA), iron chelator (1,10-phenanthroline), or copper(I) chelator (neocuprin) did not decrease CSE-induced protein carbonylation in THP-1 cells. These results suggest that protein carbonylation is induced by CSE in THP-1 cells via a copper(II)-catalyzed reaction and not an iron-catalyzed reaction. Furthermore, the copper(II) ions involved in this CSE-induced protein carbonylation are derived from the intracellular pool, not via uptake from the extracellular medium. We speculate that natural copper(II) chelators may prevent some of the health problems caused by cigarette smoking, including lung disease, renal failure, and diabetes.
Chemical Research in Toxicology 06/2009; 22(7):1232-8. · 3.78 Impact Factor
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ABSTRACT: Epidemiologic studies have shown a strong association between cigarette smoking and cardiovascular diseases. Various oxidative species and free radicals are produced during cigarette smoking and these lead to endothelial dysfunction and inflammation. Expression of adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), E-selectin, and vascular cell adhesion molecule-1, and adhesion of leukocytes are present in atherosclerosis. We showed previously that a nonfractionated cigarette smoke extract (CSE) induces surface expression of ICAM-1 and E-selectin in human umbilical vein endothelial cells (HUVEC). We then investigated the role of the MAPKs (ERK1/2, JNK, and p38) and AP-1 and the role of actin cytoskeleton reorganization in the CSE-induced expression of ICAM-1 and E-selectin. Western blot analysis showed that CSE treatment rapidly and significantly caused phosphorylation of JNK and ERK1/2 but not of p38. Cytochalasin D (an actin filament disruptor) partially inhibited CSE-induced ICAM-1 and E-selectin surface expression. However, inhibitors of ERK1/2 (PD98059) and JNK (SP600125) did not attenuate the CSE-induced ICAM-1 and E-selectin surface expression. The results of electrophoretic mobility shift assay showed that CSE enhanced AP-1 binding activity. Therefore, CSE activated AP-1 and upregulated ICAM-1 and E-selectin surface expression in HUVEC seem to be via an MAPK-independent pathway. Moreover, the dynamic reorganization of the actin cytoskeleton seems to be required for the CSE-induced surface expression of ICAM-1 and E-selectin.
Environmental and Molecular Mutagenesis 01/2009; 50(2):96-104. · 3.71 Impact Factor
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ABSTRACT: Inorganic arsenic is a known human carcinogen, yet its mechanism of action remains unclear. Our previous study showed that arsenite significantly induces oxidative DNA adducts and DNA-protein cross-links in several mammalian cell lines. In the present study, we used the random amplified polymorphic DNA (RAPD) assay to evaluate the possible target in the genomic DNA of human lymphoblastoid cells that were exposed to sodium arsenite. Treatment with both 10 and 80 microM arsenite for 4h induced significant changes in RAPD profiles compared with the control pattern. Two 10-mer RAPD primers (D11 and F1) produced the most distinguishable banding profiles between arsenite-treated and control genomic DNA. The sequencing of four arsenite-sensitive RAPD bands showed that the RB1CC1 and PACE4 genes might be the DNA targets of sodium arsenite treatment. We propose that arsenite may induce sequence- or gene-specific damage and then change the RAPD profile in human lymphoblastoid cells. The results of our study also show that RAPD combined with other techniques is a good tool for detecting alterations in genomic DNA and for the direct screening of new molecular markers related to arsenite-induced carcinogenesis.
Toxicology 10/2007; 239(1-2):108-15. · 3.68 Impact Factor
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ABSTRACT: In the present study, we compared the anti-Fenton reaction activity of three taxa of water yam (Dioscorea alata L.): DS2, TN2 and PSY [D. alata L. var. purpurea (Roxb.) M. Pouch]. Anti-Fenton reaction activity was evaluated by measuring the damage inflicted on calf thymus DNA by copper ions combined with hydrogen peroxide with the use of an ethidium bromide binding assay and agarose gel electrophoresis. We found that extracts of tuber pulp from all three taxa of yam had significant anti-Fenton reaction activity. The protection pattern of the three tuber pulp extracts was similar to that of EDTA, a typical divalent metal ion chelator, which displayed a significant protection lag-phase. With the use of thin-layer chromatography, we found that a common, major ansialdehyde-sulphuric acid stained spot (possibly a polysaccharide mucilage) with an Rf of 0.09 may be the most likely contributor to the anti-Fenton reaction activities of the yam tuber extracts investigated. The present study identifies the mechanism of the health benefit of the Dioscorea family. The copper-chelating and absorbing capability of yam tuber pulp extracts may be useful in functional screening.
International Journal of Food Science & Technology 05/2007; 42(9):1107 - 1113. · 1.26 Impact Factor
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ABSTRACT: To evaluate the effect of garlic-containing medium on the antioxidant activity of liquid-state fermentation products of Monascus spp., antioxidant activity of garlic extract (GA), extract from mycelia of Monascus pilosus mutant submerged culture (MP), extract from mycelia of M. pilosus mutant submerged garlic-containing culture (MPG), and growth substrate of M. pilosus mutant submerged garlic-containing culture (SMPG) was evaluated by various antioxidant assays, including DPPH (1,1-diphenyl-2-picryl-hydrazyl), superoxide- and hydrogen peroxide-scavenging assays, lipid peroxidation assay, and metal-binding assay as well as ethidium bromide fluorescence-binding assay. The results showed that radical-scavenging, iron-chelating, and DNA-protection activities of GA were significantly higher than MP; however, after culturing in garlic-containing medium, the antioxidant activities of M. pilosus fermentation products MPG and SMPG were significantly increased but not more than GA. The results imply that addition of garlic paste into culture medium raised the nutritive quality of M. pilosus fermentation products by increasing antioxidant activity.
Journal of Food Science 07/2006; 71(6):S456 - S460. · 1.66 Impact Factor
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ABSTRACT: Cigarette smoke is a major risk factor for human diseases, such as lung cancer and atherosclerosis. The present study was undertaken to investigate the effect of non-fractionated water-soluble cigarette smoke extract (NFWS CSE) on DNA damage and cellular adhesion molecule expression in human umbilical vein endothelial cells (HUVECs). DNA damage and the surface expression of intercellular adhesion molecule-1 (ICAM-1) and E-selectin were determined by the use of the comet assay and flow cytometry, respectively. NFWS CSE-induced DNA damage in a dose-dependent manner during a 2 h exposure. Pretreatment with ascorbic acid or alpha-tocopherol completely inhibited the NFWS CSE-induced DNA damage. NFWS CSE exposure also up-regulated the surface expression of ICAM-1 and E-selectin in HUVECs. Pretreatment with ascorbic acid or alpha-tocopherol had no effect on NFWS CSE-induced E-selectin and ICAM-1 expression. In contrast, the non-antioxidant metal chelator 1,10-phenanthroline partially suppressed the surface expression of ICAM-1 and E-selectin. These results suggest that NFWS CSE exposure induces both DNA damage and the surface expression of adhesion molecules in HUVECs. However, the molecular mechanism of these effects may be through different pathways: reactive oxygen species are involved in NFWS CSE-induced DNA damage but have little relation to NFWS CSE-induced E-selectin and ICAM-1 expression.
Chemico-Biological Interactions 01/2005; 150(3):233-41. · 2.46 Impact Factor
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ABSTRACT: The rhizome extract of Dioscorea has been shown to possess radical scavenging activity. In this study, the protective effect of water yam (Dioscorea alata L.) rhizome extract on calf thymus DNA and plasmid DNA strand breakage by the copper-driven Fenton reaction and X-irradiation was examined. The protective activity in vitro of four lyophilized extracts obtained from yam rhizomes: (1) aqueous extract (YAE); (2) 30% ethanolic extract (YEE); (3) aqueous extract boiled for 30 min (BYAE); and (4) 30% ethanolic extract boiled for 30 min (BYEE) were evaluated by ethidium bromide binding assay and DNA nicking assay. The YAE, YEE, and BYEE effectively inhibited the copper-driven Fenton reaction-induced damage of calf thymus DNA, while inhibition was less pronounced in the case of X-ray induced strand breakage of plasmid DNA. While BYAE potently inhibited X-ray induced strand breaks in plasmid pGL3 DNA, it failed to inhibit, and even greatly enhanced copper-H(2)O(2) induced damage of calf thymus DNA. The present results demonstrate strong copper chelating and weak hydroxyl radical scavenging activities in yam rhizome extracts, and these activities may vary depending on the procedures used in preparing the extract.
Phytotherapy Research 05/2004; 18(4):325-8. · 2.09 Impact Factor
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ABSTRACT: Arsenic is recognized to be a nonmutagenic carcinogen because it induces DNA damage only at very high concentrations. However, many more DNA strand breaks could be detected by digesting the DNA of arsenite-treated cells with endonuclease III, formamidopyrimidine-DNA glycosylase, and proteinase K. By doing so, arsenite could be shown to induce DNA damage in human cells within a pathologically meaningful concentration range. Oxidized guanine products were detected in all arsenite-treated human cells examined. DNA-protein cross-links were also detected in arsenite-treated NB4 and HL60 cells. In human umbilical vein endothelial cells, the induction of oxidized guanine products by arsenite was sensitive to inhibitors of nitric oxide (NO) synthase but not to oxidant modulators, whereas the opposite result was obtained in vascular smooth muscle cells. On the other hand, the arsenite-induced oxidized guanine products and DNA-protein cross-links in NB4 and HL60 cells were sensitive to modulators of calcium, NO synthase, oxidant, and myeloperoxidase. Therefore, although oxidized guanine products were detected in all the human cells treated with arsenite, the pathways could be different in different cell types. Because the sensitivity and the mechanism of arsenic intoxication are cell specific, it is important that target tissues and target cells are used for investigations. It is also important that pathologically or pharmacologically meaningful concentrations of arsenic are used. This is because in most cases we are dealing with the chronic effect rather than acute toxicity.
Environmental Health Perspectives 11/2002; 110 Suppl 5:753-6. · 7.04 Impact Factor
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ABSTRACT: We report here that sequential digestion with endonuclease III, formamidopyrimidine-DNA glycosylase, and proteinase K in Tris buffer markedly increased the sensitivity for detecting DNA damage in arsenic-treated cells. These three enzymes increased DNA strand breaks in an additive manner. By using this sequential-enzyme-digestion comet assay, we demonstrated that trivalent inorganic arsenic induced more DNA damage than monomethylarsonous acid, monomethylarsonic acid, and dimethylarsinic acid in human blood cell lines. However, trivalent inorganic arsenic was far less potent than monomethylarsonous acid in inhibiting pyruvate dehydrogenase activity. Therefore, different mechanisms are involved in inhibiting pyruvate dehydrogenase activity and inducing DNA damage. Our results also indicate while trivalent inorganic arsenic induced more endonuclease III-digestible adducts, monomethylarsonous acid and monomethylarsonic acid induced more proteinase K-digestible adducts. These results suggest there is a difference in the mechanism for inducing DNA damage between inorganic and organic methylated arsenic compounds.
Chemical Research in Toxicology 11/2002; 15(10):1254-8. · 3.78 Impact Factor
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ABSTRACT: Inorganic arsenic is a known human carcinogen, yet its mechanism of action remains unclear. Our previous study showed that arsenite significantly induces oxidative DNA adducts and DNA–protein cross-links in several mammalian cell lines. In the present study, we used the random amplified polymorphic DNA (RAPD) assay to evaluate the possible target in the genomic DNA of human lymphoblastoid cells that were exposed to sodium arsenite. Treatment with both 10 and 80 μM arsenite for 4 h induced significant changes in RAPD profiles compared with the control pattern. Two 10-mer RAPD primers (D11 and F1) produced the most distinguishable banding profiles between arsenite-treated and control genomic DNA. The sequencing of four arsenite-sensitive RAPD bands showed that the RB1CC1 and PACE4 genes might be the DNA targets of sodium arsenite treatment. We propose that arsenite may induce sequence- or gene-specific damage and then change the RAPD profile in human lymphoblastoid cells. The results of our study also show that RAPD combined with other techniques is a good tool for detecting alterations in genomic DNA and for the direct screening of new molecular markers related to arsenite-induced carcinogenesis.
Toxicology.
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ABSTRACT: Because lymphocytes from fragile X patients have been reported as hypersensitive to bleomycin-induced chromatid breaks and because the number of trinucleotide repeats in families with fragile X syndrome has a propensity to expand, we have investigated the possibility that fragile X cells may be hypersensitive to DNA damage and have a lower capacity for DNA repair.
Lymphocytes from normal and fragile X syndrome donors were immortalized by Epstein-Barr virus transformation. Characteristics of fragile X syndrome including the folate-sensitive fragile site on chromosome Xq27.3, length of CGG repeat expansion, and FMRP expression in Epstein-Barr virus-transformed lymphoblastoid cell lines were analyzed by standard cytogenetic methods, Southern blot, and Western blot, respectively. Analysis of DNA damage and repair induced by hydrogen peroxide, bleomycin, ethyl methanesulfonate, 4-nitroquinoline-N-oxide, etoposide, and mitomycin C was carried out by single-cell gel electrophoresis assay (known as comet assay).
Lymphoblastoid cell lines from fragile X donors had a folate-sensitive fragile site on chromosome Xq27.3, no or low FMRP expression, and expansion of the CGG repeat. Results of comet assay showed that fragile X cells were not more sensitive to mutagen-induced DNA strand breaks and did not have lower DNA repair capacity in comparison with normal cells. Furthermore, one fragile X cell line showed hyposensitivity to DNA strand breaks induced by hydrogen peroxide, bleomycin, and ethyl methansulfonate.
The results of this study do not support the notion that CGG trinucleotide expansion in fragile X syndrome is caused by permanent deficiency in DNA repair.
Archives of Medical Research 33(2):128-35. · 1.88 Impact Factor
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ABSTRACT: The fermented products of Monascus sp. are known for their antihypercholesterolaemic effects, however, their antioxidant activities are different from those of many plant-derived foods. To evaluate the effect of ginger addition into the medium on the antioxidant activity of Monascuspilosus fermented products, we cultured uninoculated PDB medium (PDB), inoculated PDB medium (MP), uninoculated ginger-containing medium (PDBG), and inoculated ginger-containing medium (MPG). The broth and mycelia were collected, freeze-dried, and extracted to evaluate their free radical scavenging activities, inhibition of peroxidation, phenolic content, inhibition of DNA damage, cellular antioxidant activity, and expression of the antioxidant enzymes. The results showed that MPG had significantly higher antioxidant activity than PDB, MP, and PDBG at all fermentation time points. Moreover, the fermentation process significantly increased the antioxidant activities of MPG. After the inherent level of antioxidant capacity was increased, the modified M. pilosus fermented product demonstrated a higher anti-atherosclerotic value than the unmodified product.
Food Chemistry.
