The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
Frank J Gonzalez - One of the best experts on this subject based on the ideXlab platform.
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metabolic activation of Elemicin leads to the inhibition of stearoyl coa desaturase 1
Chemical Research in Toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Frank J Gonzalez, Xiuwei Yang, Yan Qu, Ting Zhang, Fei LiAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1′-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could at...
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Metabolic Activation of Elemicin Leads to the Inhibition of Stearoyl-CoA Desaturase 1.
Chemical research in toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Xiuwei Yang, Ting Zhang, Xu Zhu, Man-yun Dai, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1'-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could attenuate the susceptibility of mice to Elemicin-induced hepatomegaly. This study revealed that metabolic activation of Elemicin leads to SCD1 inhibition in liver, suggesting that upregulation of SCD1 may serve as potential intervention strategy for Elemicin-induced toxicity.
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Role of Metabolic Activation in Elemicin-Induced Cellular Toxicity
Journal of agricultural and food chemistry, 2019Co-Authors: Yikun Wang, Xuerong Xiao, Xiuwei Yang, Xiaonan Yang, Xu Zhu, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin, an alkenylbenzene constituent of natural oils of several plant species, is widely distributed in food, dietary supplements, and medicinal plants. 1'-Hydroxylation is known to cause metabolic activation of alkenylbenzenes leading to their potential toxicity. The aim of this study was to explore the relationship between Elemicin metabolism and its toxicity through comparing the metabolic maps between Elemicin and 1'-hydroxyElemicin. Elemicin was transformed into a reactive metabolite of 1'-hydroxyElemicin, which was subsequently conjugated with cysteine (Cys) and N-acetylcysteine (NAC). Administration of NAC could significantly ameliorate the Elemicin- and 1'-hydroxyElemicin-induced cytotoxicity of HepG2 cells, while depletion of Cys with diethyl maleate (DEM) increased cytotoxicity. Recombinant human CYP screening and CYP inhibition experiments revealed that multiple CYPs, notably CYP1A1, CYP1A2, and CYP3A4, were responsible for the metabolic activation of Elemicin. This study revealed that metabolic activation plays a critical role in Elemicin cytotoxicity.
Xiaonan Yang - One of the best experts on this subject based on the ideXlab platform.
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metabolic activation of Elemicin leads to the inhibition of stearoyl coa desaturase 1
Chemical Research in Toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Frank J Gonzalez, Xiuwei Yang, Yan Qu, Ting Zhang, Fei LiAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1′-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could at...
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Metabolic Activation of Elemicin Leads to the Inhibition of Stearoyl-CoA Desaturase 1.
Chemical research in toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Xiuwei Yang, Ting Zhang, Xu Zhu, Man-yun Dai, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1'-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could attenuate the susceptibility of mice to Elemicin-induced hepatomegaly. This study revealed that metabolic activation of Elemicin leads to SCD1 inhibition in liver, suggesting that upregulation of SCD1 may serve as potential intervention strategy for Elemicin-induced toxicity.
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Role of Metabolic Activation in Elemicin-Induced Cellular Toxicity
Journal of agricultural and food chemistry, 2019Co-Authors: Yikun Wang, Xuerong Xiao, Xiuwei Yang, Xiaonan Yang, Xu Zhu, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin, an alkenylbenzene constituent of natural oils of several plant species, is widely distributed in food, dietary supplements, and medicinal plants. 1'-Hydroxylation is known to cause metabolic activation of alkenylbenzenes leading to their potential toxicity. The aim of this study was to explore the relationship between Elemicin metabolism and its toxicity through comparing the metabolic maps between Elemicin and 1'-hydroxyElemicin. Elemicin was transformed into a reactive metabolite of 1'-hydroxyElemicin, which was subsequently conjugated with cysteine (Cys) and N-acetylcysteine (NAC). Administration of NAC could significantly ameliorate the Elemicin- and 1'-hydroxyElemicin-induced cytotoxicity of HepG2 cells, while depletion of Cys with diethyl maleate (DEM) increased cytotoxicity. Recombinant human CYP screening and CYP inhibition experiments revealed that multiple CYPs, notably CYP1A1, CYP1A2, and CYP3A4, were responsible for the metabolic activation of Elemicin. This study revealed that metabolic activation plays a critical role in Elemicin cytotoxicity.
Yikun Wang - One of the best experts on this subject based on the ideXlab platform.
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metabolic activation of Elemicin leads to the inhibition of stearoyl coa desaturase 1
Chemical Research in Toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Frank J Gonzalez, Xiuwei Yang, Yan Qu, Ting Zhang, Fei LiAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1′-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could at...
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Metabolic Activation of Elemicin Leads to the Inhibition of Stearoyl-CoA Desaturase 1.
Chemical research in toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Xiuwei Yang, Ting Zhang, Xu Zhu, Man-yun Dai, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1'-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could attenuate the susceptibility of mice to Elemicin-induced hepatomegaly. This study revealed that metabolic activation of Elemicin leads to SCD1 inhibition in liver, suggesting that upregulation of SCD1 may serve as potential intervention strategy for Elemicin-induced toxicity.
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Role of Metabolic Activation in Elemicin-Induced Cellular Toxicity
Journal of agricultural and food chemistry, 2019Co-Authors: Yikun Wang, Xuerong Xiao, Xiuwei Yang, Xiaonan Yang, Xu Zhu, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin, an alkenylbenzene constituent of natural oils of several plant species, is widely distributed in food, dietary supplements, and medicinal plants. 1'-Hydroxylation is known to cause metabolic activation of alkenylbenzenes leading to their potential toxicity. The aim of this study was to explore the relationship between Elemicin metabolism and its toxicity through comparing the metabolic maps between Elemicin and 1'-hydroxyElemicin. Elemicin was transformed into a reactive metabolite of 1'-hydroxyElemicin, which was subsequently conjugated with cysteine (Cys) and N-acetylcysteine (NAC). Administration of NAC could significantly ameliorate the Elemicin- and 1'-hydroxyElemicin-induced cytotoxicity of HepG2 cells, while depletion of Cys with diethyl maleate (DEM) increased cytotoxicity. Recombinant human CYP screening and CYP inhibition experiments revealed that multiple CYPs, notably CYP1A1, CYP1A2, and CYP3A4, were responsible for the metabolic activation of Elemicin. This study revealed that metabolic activation plays a critical role in Elemicin cytotoxicity.
Xuerong Xiao - One of the best experts on this subject based on the ideXlab platform.
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metabolic activation of Elemicin leads to the inhibition of stearoyl coa desaturase 1
Chemical Research in Toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Frank J Gonzalez, Xiuwei Yang, Yan Qu, Ting Zhang, Fei LiAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1′-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could at...
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Metabolic Activation of Elemicin Leads to the Inhibition of Stearoyl-CoA Desaturase 1.
Chemical research in toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Xiuwei Yang, Ting Zhang, Xu Zhu, Man-yun Dai, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1'-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could attenuate the susceptibility of mice to Elemicin-induced hepatomegaly. This study revealed that metabolic activation of Elemicin leads to SCD1 inhibition in liver, suggesting that upregulation of SCD1 may serve as potential intervention strategy for Elemicin-induced toxicity.
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Role of Metabolic Activation in Elemicin-Induced Cellular Toxicity
Journal of agricultural and food chemistry, 2019Co-Authors: Yikun Wang, Xuerong Xiao, Xiuwei Yang, Xiaonan Yang, Xu Zhu, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin, an alkenylbenzene constituent of natural oils of several plant species, is widely distributed in food, dietary supplements, and medicinal plants. 1'-Hydroxylation is known to cause metabolic activation of alkenylbenzenes leading to their potential toxicity. The aim of this study was to explore the relationship between Elemicin metabolism and its toxicity through comparing the metabolic maps between Elemicin and 1'-hydroxyElemicin. Elemicin was transformed into a reactive metabolite of 1'-hydroxyElemicin, which was subsequently conjugated with cysteine (Cys) and N-acetylcysteine (NAC). Administration of NAC could significantly ameliorate the Elemicin- and 1'-hydroxyElemicin-induced cytotoxicity of HepG2 cells, while depletion of Cys with diethyl maleate (DEM) increased cytotoxicity. Recombinant human CYP screening and CYP inhibition experiments revealed that multiple CYPs, notably CYP1A1, CYP1A2, and CYP3A4, were responsible for the metabolic activation of Elemicin. This study revealed that metabolic activation plays a critical role in Elemicin cytotoxicity.
Xiuwei Yang - One of the best experts on this subject based on the ideXlab platform.
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metabolic activation of Elemicin leads to the inhibition of stearoyl coa desaturase 1
Chemical Research in Toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Frank J Gonzalez, Xiuwei Yang, Yan Qu, Ting Zhang, Fei LiAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1′-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could at...
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Metabolic Activation of Elemicin Leads to the Inhibition of Stearoyl-CoA Desaturase 1.
Chemical research in toxicology, 2019Co-Authors: Xiaonan Yang, Xuerong Xiao, Yikun Wang, Xiuwei Yang, Ting Zhang, Xu Zhu, Man-yun Dai, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin is a constituent of natural aromatic phenylpropanoids present in many herbs and spices. However, its potential to cause toxicity remains unclear. To examine the potential toxicity and associated mechanism, Elemicin was administered to mice for 3 weeks and serum metabolites were examined. Enlarged livers were observed in Elemicin-treated mice, which were accompanied by lower ratios of unsaturated- and saturated-lysophosphatidylcholines in plasma, and inhibition of stearoyl-CoA desaturase 1 (Scd1) mRNA expression in liver. Administration of the unsaturated fatty acid oleic acid reduced the toxicity of 1'-hydroxylElemicin, the primary oxidative metabolite of Elemicin, while treatment with the SCD1 inhibitor A939572 potentiated its toxicity. Furthermore, the in vitro use of recombinant human CYPs and chemical inhibition of CYPs in human liver microsomes revealed that CYP1A1 and CYP1A2 were the primary CYPs responsible for Elemicin bioactivation. Notably, the CYP1A2 inhibitor α-naphthoflavone could attenuate the susceptibility of mice to Elemicin-induced hepatomegaly. This study revealed that metabolic activation of Elemicin leads to SCD1 inhibition in liver, suggesting that upregulation of SCD1 may serve as potential intervention strategy for Elemicin-induced toxicity.
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Role of Metabolic Activation in Elemicin-Induced Cellular Toxicity
Journal of agricultural and food chemistry, 2019Co-Authors: Yikun Wang, Xuerong Xiao, Xiuwei Yang, Xiaonan Yang, Xu Zhu, Hong-bo Qin, Frank J GonzalezAbstract:Elemicin, an alkenylbenzene constituent of natural oils of several plant species, is widely distributed in food, dietary supplements, and medicinal plants. 1'-Hydroxylation is known to cause metabolic activation of alkenylbenzenes leading to their potential toxicity. The aim of this study was to explore the relationship between Elemicin metabolism and its toxicity through comparing the metabolic maps between Elemicin and 1'-hydroxyElemicin. Elemicin was transformed into a reactive metabolite of 1'-hydroxyElemicin, which was subsequently conjugated with cysteine (Cys) and N-acetylcysteine (NAC). Administration of NAC could significantly ameliorate the Elemicin- and 1'-hydroxyElemicin-induced cytotoxicity of HepG2 cells, while depletion of Cys with diethyl maleate (DEM) increased cytotoxicity. Recombinant human CYP screening and CYP inhibition experiments revealed that multiple CYPs, notably CYP1A1, CYP1A2, and CYP3A4, were responsible for the metabolic activation of Elemicin. This study revealed that metabolic activation plays a critical role in Elemicin cytotoxicity.