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( Seo Y. Go ),( Kyoung J. Kwon ),( Sue N. Park ),( Yhun Y. Sheen ) 한국응용약물학회 2007 Biomolecules & Therapeutics(구 응용약물학회지) Vol.15 No.3
Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a major constituent of rhubarb. Although it has been claimed to have a wild spectrum of therapeutic value, its side effects, especially in human kidney cells have not been well characterized. In this study, we have carried out in vitro genetic toxicity test of emodin and microarray analysis of differentially expressed genes in response to emodin. The result of Ames test showed mutations with emodin treatment in base substitution strain TA1535 both with and without exogenous metabolic activation. Likewise, emodin showed mutations in frame shift TA98 both with and without exogenous metabolic activation. The result of COMET assay in L5178Y cells with emodin treatment showed DNA damage both with and without exogenous metabolic activation. Emodin did not increase micronuclei in CHO cells both with and without exogenous metabolic activation. 150 Genes were selected as differentially expressed genes in response to emodin by microarray analysis and these genes would be candidate biomarkers of genetic toxic action of emodin.
Go, Seo-Y.,Kwon, Kyoung-J.,Park, Sue-N.,Sheen, Yhun-Y. The Korean Society of Applied Pharmacology 2007 Biomolecules & Therapeutics(구 응용약물학회지) Vol. No.
Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a major constituent of rhubarb. Although it has been claimed to have a wild spectrum of therapeutic value, its side effects, especially in human kidney cells have not been well characterized. In this study, we have carried out in vitro genetic toxicity test of emodin and microarray analysis of differentially expressed genes in response to emodin. The result of Ames test showed mutations with emodin treatment in base substitution strain TA1535 both with and without exogenous metabolic activation. Likewise, emodin showed mutations in frame shift TA98 both with and without exogenous metabolic activation. The result of COMET assay in L5178Y cells with emodin treatment showed DNA damage both with and without exogenous metabolic activation. Emodin did not increase micronuclei in CHO cells both with and without exogenous metabolic activation. 150 Genes were selected as differentially expressed genes in response to emodin by microarray analysis and these genes would be candidate biomarkers of genetic toxic action of emodin.
( Sue N. Park ),( Yhun Y. Sheen ),( Ki Y. Kim ),( Ji H. Kim ),( Kyoung J. Kwon ),( Seo Y. Go ),( Kyung N. Min ),( Woo S. Lee ) 한국응용약물학회 2006 Biomolecules & Therapeutics(구 응용약물학회지) Vol.14 No.4
1,2-Dibromoethane (DBE) has been widely used as a soil fumigant, an additive to leaded gasoline and an industrial solvent. In this study, we have carried out in vitro genetic toxicity test of 1,2-dibromoethane and microarray analysis of differentially expressed genes in response to 1,2-dibromoethane. 1,2-Dibromoethane showed mutations in base substitution strain TA1535 both with and without exogenous metabolic activation. 1,2-Dibromoethane showed mutations in frame shift TA98 both with and without exogenous metabolic activation. 1,2-Dibromoethane showed DNA damage based on single cell gel/comet assay in L5178Y cells both with and without exogenous metabolic activation. 1,2-Dibromoethane increased micronuclei in CHO cells both with and without exogenous metabolic activation. Microarray analysis of gene expression profiles in L5l78Y cells in response to 1,2-dibromoethane selected differentially expressed 241 genes that would be candidate biomarkers of genetic toxic action of 1,2-dibromoethane.
Genetic Toxicity Test of Methylcarbamate by Ames, Micronucleus, Comet Assays and Microarray Analysis
( Kyoung J. Kwon ),( Seo Y. Go ),( Sue N. Park ),( Yhun Y. Sheen ) 한국응용약물학회 2007 Biomolecules & Therapeutics(구 응용약물학회지) Vol.15 No.3
Carbamates have excellent insecticidal activities against a broad spectrum of insects. They possess knocking-down, fast-killing, and systemic effects, however, they are toxic to mammals. In this study, we have carried out in vitro genetic toxicity test of methylcarbamate and microarray analysis of differentially expressed genes in response to methylcarbamate. Methylcarbamate did not show mutations in base substitution strain TA1535 both with and without exogenous metabolic activation. Methylcarbamate did not show mutations in frame shift TA98 both with and without exogenous metabolic activation. Methylcarbamate showed DNA damage based on single cell gel/comet assay in L5178Y cells both with and without exogenous metabolic activation. Methylcarbamate did not increase micronuclei in CHO cells both with and without exogenous metabolic activation. Microarray analysis of gene expression profiles in L5178Y cells in response to methylcarbamate selected differentially expressed 132 genes that could be candidate biomarkers of genetic toxic action of methylcarbamate.
Genetic Toxicity Test of Methylcarbamate by Ames, Micronucleus, Comet Assays and Microarray Analysis
Kwon, Kyoung-J.,Go, Seo-Y.,Park, Sue-N.,Sheen, Yhun-Y. The Korean Society of Applied Pharmacology 2007 Biomolecules & Therapeutics(구 응용약물학회지) Vol. No.
Carbamates have excellent insecticidal activities against a broad spectrum of insects. They possess knocking-down, fast-killing, and systemic effects, however, they are toxic to mammals. In this study, we have carried out in vitro genetic toxicity test of methylcarbamate and microarray analysis of differentially expressed genes in response to methylcarbamate. Methylcarbamate did not show mutations in base substitution strain TA1535 both with and without exogenous metabolic activation. Methylcarbamate did not show mutations in frame shift TA98 both with and without exogenous metabolic activation. Methylcarbamate showed DNA damage based on single cell gel/comet assay in L5178Y cells both with and without exogenous metabolic activation. Methylcarbamate did not increase micronuclei in CHO cells both with and without exogenous metabolic activation. Microarray analysis of gene expression profiles in L5178Y cells in response to methylcarbamate selected differentially expressed 132 genes that could be candidate biomarkers of genetic toxic action of methylcarbamate.
Genetic Toxicity Test of Glycidol by Ames, Micronucleus, Comet Assays and Microarray Analysis
( Ji H. Kim ),( Ki Y. Kim ),( Kyoung J. Kwon ),( Seo Y. Go ),( Kyung N. Min ),( Woo S. Lee ),( Sue N. Park ),( Yhun Y. Sheen ) 한국응용약물학회 2006 Biomolecules & Therapeutics(구 응용약물학회지) Vol.14 No.4
The primary use for glycidol is as a stabilizer in the manufacture of vinylpolymers, however, it is also used as an intermediate in the production of pharmaceuticals, as an additives for oil and synthetic hydraulic fluids, and as a diluting agent is same epoxy resins. In this study, we have carried out in vitro genetic toxicity test of glycidol and microarray analysis of differentially expressed genes in response to glycidol. The result of Ames test showed mutations with glycidol treatment in base substitution strain TA1535 both with and without exogenous metabolic activation. Likewise, glycidol showed mutations in frame shift TA98 both with and without exogenous metabolic activation. The result of COMET assay in L5l78Y cells with glycidol treatment showed DNA damage both with and without exogenous metabolic activation. Glycidol increased micronuclei in CHO cells both with and without exogenous metabolic activation. 150 Genes were selected as differentially expressed genes in response to glycidol by microarray analysis and these genes would be candidate biomarkers of genetic toxic action of glycidol.
An isoflavone compound daidzein elicits myoblast differentiation and myotube growth
Lee, S.J.,Vuong, T.A.,Go, G.Y.,Song, Y.J.,Lee, S.,Lee, S.Y.,Kim, S.W.,Lee, J.,Kim, Y.K.,Seo, D.W.,Kim, K.H.,Kang, J.S.,Bae, G.U. ELSEVIER SCIENCE B.V.; AMSTERDAM 2017 JOURNAL OF FUNCTIONAL FOODS Vol.38 No.1
Preservation of muscle stem cell function is critical for muscle homeostasis and the regenerative capacity of stem cells declines with age, leading to muscle loss. Previously, daidzein, a natural isoflavone from Leguminosae, has been shown to prevent TNF-α-induced muscle atrophy. However, the molecular mechanisms of daidzein in these processes are currently unknown. In this study, we demonstrate a positive effect of black soybean extract (BS Ext) and daidzein on myoblast differentiation and myotube growth. Daidzein prevents dexamethasone-induced myotube atrophy through Akt activation. The promyogenic effect of BS Ext and daidzein is mediated through two promyogenic kinases, Akt and p38MAPK that in turn activates a key myogenic transcription factor MyoD. Additionally, BS Ext and daidzein promote myotube growth through Akt/mTOR/S6K pathway. Finally, daidzein augments MyoD-dependent myogenic conversion of mouse embryonic fibroblasts. Taken together, our data suggest that daidzein promotes myogenic differentiation and myotube hypertrophy through p38 and Akt/mTOR/S6K pathway.