2014•Chinese Journal of Control of Endemic DiseasesRequires access

Induction of various arsenide on antioxidase in Chang liver cells

Gao Shuan

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Abstract

Objectives To explore different organic and inorganic arsenics toxicity in Chang liver cells and the induction on phaseⅡdetoxifying enzymes and antioxidant enzyme protein. Methods Alamar Blue reduction method was used to evaluate cell viability; Western blot analysis was used to detect the protein expression levels of HO- 1,NQO1,GST and GR in cells. Results Through the Alamar Blue determination of cell proliferation activity,we found the toxic size of As2O3 NaAsO2 Na2HAsO4 DMA; Different concentrations of inorganic arsenic exposure Chang liver cells for 6h,protein expression levels of HO- 1 and NQO1 gradually increased; GST and GR protein expression had nothing to do with exposure concentration,three groups shared the same expression level. While,the organic arsenic DMA was totally opposite; as the exposure concentration elevated,GST and GR protein expression levels gradually increased,the protein expression of HO- 1and NQO1 had nothing to do with exposure concentration. Exposure group and control group had no difference. Conclusion Different arsenide had different toxic effect on the Chang liver cells. Different organic and inorganic arsenic have different induced intensity for phaseⅡdetoxifying enzymes and antioxidant enzymes expression.

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Objectives To explore different organic and inorganic arsenics toxicity in Chang liver cells and the induction on phaseⅡdetoxifying enzymes and antioxidant enzyme protein. Methods Alamar Blue reduction method was used to evaluate cell viability; Western blot analysis was used to detect the protein expression levels of HO- 1,NQO1,GST and GR in cells. Results Through the Alamar Blue determination of cell proliferation activity,we found the toxic size of As2O3 NaAsO2 Na2HAsO4 DMA; Different concentrations of inorganic arsenic exposure Chang liver cells for 6h,protein expression levels of HO- 1 and NQO1 gradually increased; GST and GR protein expression had nothing to do with exposure concentration,three groups shared the same expression level. While,the organic arsenic DMA was totally opposite; as the exposure concentration elevated,GST and GR protein expression levels gradually increased,the protein expression of HO- 1and NQO1 had nothing to do with exposure concentration. Exposure group and control group had no difference. Conclusion Different arsenide had different toxic effect on the Chang liver cells. Different organic and inorganic arsenic have different induced intensity for phaseⅡdetoxifying enzymes and antioxidant enzymes expression.

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Available abstract

Objectives To explore different organic and inorganic arsenics toxicity in Chang liver cells and the induction on phaseⅡdetoxifying enzymes and antioxidant enzyme protein. Methods Alamar Blue reduction method was used to evaluate cell viability; Western blot analysis was used to detect the protein expression levels of HO- 1,NQO1,GST and GR in cells. Results Through the Alamar Blue determination of cell proliferation activity,we found the toxic size of As2O3 NaAsO2 Na2HAsO4 DMA; Different concentrations of inorganic arsenic exposure Chang liver cells for 6h,protein expression levels of HO- 1 and NQO1 gradually increased; GST and GR protein expression had nothing to do with exposure concentration,three groups shared the same expression level. While,the organic arsenic DMA was totally opposite; as the exposure concentration elevated,GST and GR protein expression levels gradually increased,the protein expression of HO- 1and NQO1 had nothing to do with exposure concentration. Exposure group and control group had no difference. Conclusion Different arsenide had different toxic effect on the Chang liver cells. Different organic and inorganic arsenic have different induced intensity for phaseⅡdetoxifying enzymes and antioxidant enzymes expression.

Key concepts: Enzyme, Western blot, Chemistry, Arsenic, Cell, Arsenic toxicity, Antioxidant, Biochemistry

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