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Wafa Kharroubi - One of the best experts on this subject based on the ideXlab platform.

  • Mitochondrial dysfunction, oxidative stress and apoptotic induction in microglial BV-2 cells treated with Sodium Arsenate.
    Journal of Environmental Sciences, 2017
    Co-Authors: Wafa Kharroubi, Samia Haj Ahmed, Thomas Nury, Pierre Andreoletti, Rachid Sakly, Mohamed Hammami, Gérard Lizard
    Abstract:

    The treatment of microglial BV-2 cells with Sodium Arsenate (As(V): 0.1-400μmol/L - 48hr) induces a dose-dependent response. The neurotoxic effects of high concentrations of As(V) (100, 200 and 400μmol/L) are characterized by increased levels of mitochondrial complexes I, II, and IV followed by increased superoxide anion generation. Moreover, As(V) triggers an apoptotic mode of cell death, demonstrated by an apoptotic SubG1 peak, associated with an alteration of plasma membrane integrity. There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP. It is therefore tempting to speculate that As(V) triggers mitochondrial dysfunction, which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage, which in turn induces an apoptotic mode of cell death.

  • Evidence of hormesis on human neuronal SK-N-BE cells treated with Sodium Arsenate: impact at the mitochondrial level.
    Environmental Science and Pollution Research, 2016
    Co-Authors: Wafa Kharroubi, Thomas Nury, Pierre Andreoletti, Rachid Sakly, Mohamed Hammami, Samia Haj Ahmed, Zohra Haouas, Amira Zarrouk, Gérard Lizard
    Abstract:

    Exposure of human neuronal SK-N-BE cells to Sodium Arsenate (AsV 0.1-400 μM; 48 h) induced a biphasic toxic effect evoking hormesis. Indeed, at low concentrations, AsV stimulates cell proliferation visualized by phase contrast microscopy, whereas at high concentrations, an induction of cell death associated with a loss of cell adhesion was observed. These side effects were confirmed with crystal violet test, cell cycle analysis, evaluation of the percentage of Ki67 positive cells, and staining with propidium iodide. The impact of AsV on mitochondrial functions, which was determined by the MTT assay, the measurement of mitochondrial transmembrane potential with DiOC6(3), and the rate of mitochondrial ATP, also support an hormesis process. In addition, in the presence of high concentrations of AsV, a significant decrease of the protein expression of OXPHOS complexes of the respiratory chain was observed by western blot supporting that AsV-induced cell death is associated with mitochondrial alterations. Therefore, there are some evidences of hormesis on AsV-treated SK-N-BE cells, and at high concentrations, the mitochondria are a target of toxicity induced by AsV.

  • Sodium Arsenate induce changes in fatty acids profiles and oxidative damage in kidney of rats
    Environmental Science and Pollution Research, 2014
    Co-Authors: Wafa Kharroubi, Mohamed Hammami, Zohra Haouas, Madiha Dhibi, Imed Chreif, Fadoua Neffati, Manel Mekni, Rachid Sakly
    Abstract:

    Six groups of rats (n = 10 per group) were exposed to 1 and 10 mg/l of Sodium Arsenate for 45 and 90 days. Kidneys from treated groups exposed to arsenic showed higher levels of trans isomers of oleic and linoleic acids as trans C181n-9, trans C18:1n-11, and trans C18:2n-6 isomers. However, a significant decrease in eicosenoic (C20:1n-9) and arachidonic (C20:4n-6) acids were observed in treated rats. Moreover, the “Δ5 desaturase index” and the saturated/polyunsaturated fatty acids ratio were increased. There was a significant increase in the level of malondialdehyde at 10 mg/l of treatment and in the amount of conjugated dienes after 90 days (p < 0.05). Significant kidney damage was observed at 10 mg/l by increase of plasma marker enzymes. Histological studies on the ultrastructure changes of kidney supported the toxic effect of Arsenate exposure. Arsenate intoxication activates significantly the superoxide dismutase at 10 mg/l for 90 days, whereas the catalase activity was markedly inhibited in all treated groups (p < 0.05). In addition, glutathione peroxidase activity was significantly increased at 45 days and dramatically declined after 90 days at 10 mg/l (p < 0.05). A significant increase in the level of glutathione was marked for the groups treated for 45 and 90 days at 1 mg/l followed by a significant decrease for rats exposed to 10 mg/l for 90 days. An increase in the level of protein carbonyl was observed in all treated groups (p < 0.05). In conclusion, the present study provides evidence for a direct effect of Arsenate on fatty acid (FA) metabolism which concerns the synthesis pathway of n-6 polyunsaturated fatty acids and leads to an increase in the trans FAs isomers. Therefore, FA-induced Arsenate kidney damage could contribute to trigger kidney cancer.

  • effects of Sodium Arsenate exposure on liver fatty acid profiles and oxidative stress in rats
    Environmental Science and Pollution Research, 2014
    Co-Authors: Wafa Kharroubi, Mohamed Hammami, Zohra Haouas, Madiha Dhibi, Imed Chreif, Fadoua Neffati, Rachid Sakly
    Abstract:

    The present study aimed to evaluate the effect of arsenic on liver fatty acids (FA) composition, hepatotoxicity and oxidative status markers in rats. Male rats were randomly devised to six groups (n = 10 per group) and exposed to Sodium Arsenate at a dose of 1 and 10 mg/l for 45 and 90 days. Arsenate exposure is associated with significant changes in the FA composition in liver. A significant increase of saturated fatty acids (SFA) in all treated groups (p < 0.01) and trans unsaturated fatty acids (trans UFA) in rats exposed both for short term for 10 mg/l (p < 0.05) and long term for 1 and 10 mg/l (p < 0.001) was observed. However, the cis UFA were significantly decreased in these groups (p < 0.05). A markedly increase of indicator in cell membrane viscosity expressed as SFA/UFA was reported in the treated groups (p < 0.001). A significant increase in the level of malondialdehyde by 38.3 % after 90 days of exposure at 10 mg/l was observed. Compared to control rats, significant liver damage was observed at 10 mg/l of Arsenate by increasing plasma marker enzymes after 90 days. It is through the histological investigations in hepatic tissues of exposed rats that these damage effects of Arsenate were confirmed. The antioxidant perturbations were observed to be more important at groups treated by the high dose (p < 0.05). An increase in the level of protein carbonyls was observed in all treated groups (p < 0.05). The present study provides evidence for a direct effect of arsenite on FA composition disturbance causing an increase of SFA and TFAs isomers, liver dysfunction and oxidative stress. Therefore, Arsenate can lead to hepatic damage and propensity towards liver cancer.

Rachid Sakly - One of the best experts on this subject based on the ideXlab platform.

  • Mitochondrial dysfunction, oxidative stress and apoptotic induction in microglial BV-2 cells treated with Sodium Arsenate.
    Journal of Environmental Sciences, 2017
    Co-Authors: Wafa Kharroubi, Samia Haj Ahmed, Thomas Nury, Pierre Andreoletti, Rachid Sakly, Mohamed Hammami, Gérard Lizard
    Abstract:

    The treatment of microglial BV-2 cells with Sodium Arsenate (As(V): 0.1-400μmol/L - 48hr) induces a dose-dependent response. The neurotoxic effects of high concentrations of As(V) (100, 200 and 400μmol/L) are characterized by increased levels of mitochondrial complexes I, II, and IV followed by increased superoxide anion generation. Moreover, As(V) triggers an apoptotic mode of cell death, demonstrated by an apoptotic SubG1 peak, associated with an alteration of plasma membrane integrity. There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP. It is therefore tempting to speculate that As(V) triggers mitochondrial dysfunction, which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage, which in turn induces an apoptotic mode of cell death.

  • Evidence of hormesis on human neuronal SK-N-BE cells treated with Sodium Arsenate: impact at the mitochondrial level.
    Environmental Science and Pollution Research, 2016
    Co-Authors: Wafa Kharroubi, Thomas Nury, Pierre Andreoletti, Rachid Sakly, Mohamed Hammami, Samia Haj Ahmed, Zohra Haouas, Amira Zarrouk, Gérard Lizard
    Abstract:

    Exposure of human neuronal SK-N-BE cells to Sodium Arsenate (AsV 0.1-400 μM; 48 h) induced a biphasic toxic effect evoking hormesis. Indeed, at low concentrations, AsV stimulates cell proliferation visualized by phase contrast microscopy, whereas at high concentrations, an induction of cell death associated with a loss of cell adhesion was observed. These side effects were confirmed with crystal violet test, cell cycle analysis, evaluation of the percentage of Ki67 positive cells, and staining with propidium iodide. The impact of AsV on mitochondrial functions, which was determined by the MTT assay, the measurement of mitochondrial transmembrane potential with DiOC6(3), and the rate of mitochondrial ATP, also support an hormesis process. In addition, in the presence of high concentrations of AsV, a significant decrease of the protein expression of OXPHOS complexes of the respiratory chain was observed by western blot supporting that AsV-induced cell death is associated with mitochondrial alterations. Therefore, there are some evidences of hormesis on AsV-treated SK-N-BE cells, and at high concentrations, the mitochondria are a target of toxicity induced by AsV.

  • Sodium Arsenate induce changes in fatty acids profiles and oxidative damage in kidney of rats
    Environmental Science and Pollution Research, 2014
    Co-Authors: Wafa Kharroubi, Mohamed Hammami, Zohra Haouas, Madiha Dhibi, Imed Chreif, Fadoua Neffati, Manel Mekni, Rachid Sakly
    Abstract:

    Six groups of rats (n = 10 per group) were exposed to 1 and 10 mg/l of Sodium Arsenate for 45 and 90 days. Kidneys from treated groups exposed to arsenic showed higher levels of trans isomers of oleic and linoleic acids as trans C181n-9, trans C18:1n-11, and trans C18:2n-6 isomers. However, a significant decrease in eicosenoic (C20:1n-9) and arachidonic (C20:4n-6) acids were observed in treated rats. Moreover, the “Δ5 desaturase index” and the saturated/polyunsaturated fatty acids ratio were increased. There was a significant increase in the level of malondialdehyde at 10 mg/l of treatment and in the amount of conjugated dienes after 90 days (p < 0.05). Significant kidney damage was observed at 10 mg/l by increase of plasma marker enzymes. Histological studies on the ultrastructure changes of kidney supported the toxic effect of Arsenate exposure. Arsenate intoxication activates significantly the superoxide dismutase at 10 mg/l for 90 days, whereas the catalase activity was markedly inhibited in all treated groups (p < 0.05). In addition, glutathione peroxidase activity was significantly increased at 45 days and dramatically declined after 90 days at 10 mg/l (p < 0.05). A significant increase in the level of glutathione was marked for the groups treated for 45 and 90 days at 1 mg/l followed by a significant decrease for rats exposed to 10 mg/l for 90 days. An increase in the level of protein carbonyl was observed in all treated groups (p < 0.05). In conclusion, the present study provides evidence for a direct effect of Arsenate on fatty acid (FA) metabolism which concerns the synthesis pathway of n-6 polyunsaturated fatty acids and leads to an increase in the trans FAs isomers. Therefore, FA-induced Arsenate kidney damage could contribute to trigger kidney cancer.

  • effects of Sodium Arsenate exposure on liver fatty acid profiles and oxidative stress in rats
    Environmental Science and Pollution Research, 2014
    Co-Authors: Wafa Kharroubi, Mohamed Hammami, Zohra Haouas, Madiha Dhibi, Imed Chreif, Fadoua Neffati, Rachid Sakly
    Abstract:

    The present study aimed to evaluate the effect of arsenic on liver fatty acids (FA) composition, hepatotoxicity and oxidative status markers in rats. Male rats were randomly devised to six groups (n = 10 per group) and exposed to Sodium Arsenate at a dose of 1 and 10 mg/l for 45 and 90 days. Arsenate exposure is associated with significant changes in the FA composition in liver. A significant increase of saturated fatty acids (SFA) in all treated groups (p < 0.01) and trans unsaturated fatty acids (trans UFA) in rats exposed both for short term for 10 mg/l (p < 0.05) and long term for 1 and 10 mg/l (p < 0.001) was observed. However, the cis UFA were significantly decreased in these groups (p < 0.05). A markedly increase of indicator in cell membrane viscosity expressed as SFA/UFA was reported in the treated groups (p < 0.001). A significant increase in the level of malondialdehyde by 38.3 % after 90 days of exposure at 10 mg/l was observed. Compared to control rats, significant liver damage was observed at 10 mg/l of Arsenate by increasing plasma marker enzymes after 90 days. It is through the histological investigations in hepatic tissues of exposed rats that these damage effects of Arsenate were confirmed. The antioxidant perturbations were observed to be more important at groups treated by the high dose (p < 0.05). An increase in the level of protein carbonyls was observed in all treated groups (p < 0.05). The present study provides evidence for a direct effect of arsenite on FA composition disturbance causing an increase of SFA and TFAs isomers, liver dysfunction and oxidative stress. Therefore, Arsenate can lead to hepatic damage and propensity towards liver cancer.

Gomes, Laise De Azevedo - One of the best experts on this subject based on the ideXlab platform.

  • Análise do crescimento e perfil bioacumulativo da cianobactéria Geitlerinema unigranulatum UFV-E01 na presença de arsenato de sódio
    2012
    Co-Authors: Gomes, Laise De Azevedo
    Abstract:

    O arsênio é um metalóide tóxico que se tornou um problema de saúde pública em todo o mundo. Como forma de reduzir a contaminação ambiental por este metalóide, a qual é proveniente de atividades antropogênicas e naturais, a utilização de microorganismos em processos de biorremediação se tem mostrado uma estratégia promissora. A cianobactéria filamentosa homocitada, Geitlerinema unigranulatum UFV-E01, pertencente à ordem Pseudanabaenales, foi isolada de um ambiente contaminado por arsênio, sugerindo uma habilidade em lidar com o efeito tóxico deste metalóide. Com vista nisso, o presente trabalho objetivou caracterizar a resistência ao arsenato de sódio e quantificar o arsênio total extracelular da cianobactéria G. unigranulatum UFV-E01. As análises de resistência ao arsenato de sódio revelaram que a cianobactéria foi capaz de crescer em até 50 mM por 20 dias. Além disso, a cianobactéria G. unigranulatum UFV-E01 acumulou arsenato de sódio por 10 dias, reduzindo em até 67% o arsênio extracelular. Pelos dados obtidos neste estudo, a cianobactéria G. unigranulatum UFV-E01 foi capaz de resistir a altas concentrações de arsenato de sódio, no entanto outras análises, como a caracterização das vias metabólicas envolvidas no processo de resistência, devem ser realizadas para considerar sua aplicação em ambientes impactados por arsênio.ABSTRACT: Arsenic is a toxic metalloid that has become a public health problem worldwide. In order to reduce the environmental contamination by this metalloid, which is derived from natural and anthropogenic activities, the use of micro-organisms in bioremediation process has shown to be a promising strategy. A filamentous homocitada cyanobacterium belonging to the order Pseudanabaenales, Geitlerinema unigranulatum UFV-E01, was isolated from an environment contaminated by arsenic, suggesting an ability to deal with the toxic effect of this metalloid. In view of this, this study aimed to characterize the resistance to Sodium Arsenate and quantify the total arsenic extracellular cyanobacterium G. unigranulatum UFV-E01. Analyses of Sodium Arsenate resistance showed that the cyanobacterium was able to grow in 50 mM for 20 days. Furthermore, the cyanobacterium G. unigranulatum UFV-E01 accumulated Sodium Arsenate for 10 days, reducing up to 67% arsenic extracellular. From the data obtained in this study, the cyanobacterium G. unigranulatum UFV-E01 was able to withstand high concentrations of Sodium Arsenate, although other analysis, the characterization of the metabolic pathways involved in the resistance must be taken to consider their use in environments impacted by arsenic

  • Análise do crescimento e perfil bioacumulativo da cianobactéria Geitlerinema unigranulatum UFV-E01 na presença de arsenato de sódio
    Programa de Pós-Graduação em Biologia Ambiental, 2012
    Co-Authors: Gomes, Laise De Azevedo
    Abstract:

    Arsenic is a toxic metalloid that has become a public health problem worldwide. In order to reduce the environmental contamination by this metalloid, which is derived from natural and anthropogenic activities, the use of micro-organisms in bioremediation process has shown to be a promising strategy. A filamentous homocitada cyanobacterium belonging to the order Pseudanabaenales, Geitlerinema unigranulatum UFV-E01, was isolated from an environment contaminated by arsenic, suggesting an ability to deal with the toxic effect of this metalloid. In view of this, this study aimed to characterize the resistance to Sodium Arsenate and quantify the total arsenic extracellular cyanobacterium G. unigranulatum UFV-E01. Analyses of Sodium Arsenate resistance showed that the cyanobacterium was able to grow in 50 mM for 20 days. Furthermore, the cyanobacterium G. unigranulatum UFV-E01 accumulated Sodium Arsenate for 10 days, reducing up to 67% arsenic extracellular. From the data obtained in this study, the cyanobacterium G. unigranulatum UFV-E01 was able to withstand high concentrations of Sodium Arsenate, although other analysis, the characterization of the metabolic pathways involved in the resistance must be taken to consider their use in environments impacted by arsenic.CNPq - Conselho Nacional de Desenvolvimento Científico e TecnológicoCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível SuperiorFAPESPA - Fundação Amazônia de Amparo a Estudos e PesquisasO arsênio é um metalóide tóxico que se tornou um problema de saúde pública em todo o mundo. Como forma de reduzir a contaminação ambiental por este metalóide, a qual é proveniente de atividades antropogênicas e naturais, a utilização de microorganismos em processos de biorremediação se tem mostrado uma estratégia promissora. A cianobactéria filamentosa homocitada, Geitlerinema unigranulatum UFV-E01, pertencente à ordem Pseudanabaenales, foi isolada de um ambiente contaminado por arsênio, sugerindo uma habilidade em lidar com o efeito tóxico deste metalóide. Com vista nisso, o presente trabalho objetivou caracterizar a resistência ao arsenato de sódio e quantificar o arsênio total extracelular da cianobactéria G. unigranulatum UFV-E01. As análises de resistência ao arsenato de sódio revelaram que a cianobactéria foi capaz de crescer em até 50 mM por 20 dias. Além disso, a cianobactéria G. unigranulatum UFV-E01 acumulou arsenato de sódio por 10 dias, reduzindo em até 67% o arsênio extracelular. Pelos dados obtidos neste estudo, a cianobactéria G. unigranulatum UFV-E01 foi capaz de resistir a altas concentrações de arsenato de sódio, no entanto outras análises, como a caracterização das vias metabólicas envolvidas no processo de resistência, devem ser realizadas para considerar sua aplicação em ambientes impactados por arsênio

Mohamed Hammami - One of the best experts on this subject based on the ideXlab platform.

  • Mitochondrial dysfunction, oxidative stress and apoptotic induction in microglial BV-2 cells treated with Sodium Arsenate.
    Journal of Environmental Sciences, 2017
    Co-Authors: Wafa Kharroubi, Samia Haj Ahmed, Thomas Nury, Pierre Andreoletti, Rachid Sakly, Mohamed Hammami, Gérard Lizard
    Abstract:

    The treatment of microglial BV-2 cells with Sodium Arsenate (As(V): 0.1-400μmol/L - 48hr) induces a dose-dependent response. The neurotoxic effects of high concentrations of As(V) (100, 200 and 400μmol/L) are characterized by increased levels of mitochondrial complexes I, II, and IV followed by increased superoxide anion generation. Moreover, As(V) triggers an apoptotic mode of cell death, demonstrated by an apoptotic SubG1 peak, associated with an alteration of plasma membrane integrity. There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP. It is therefore tempting to speculate that As(V) triggers mitochondrial dysfunction, which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage, which in turn induces an apoptotic mode of cell death.

  • Evidence of hormesis on human neuronal SK-N-BE cells treated with Sodium Arsenate: impact at the mitochondrial level.
    Environmental Science and Pollution Research, 2016
    Co-Authors: Wafa Kharroubi, Thomas Nury, Pierre Andreoletti, Rachid Sakly, Mohamed Hammami, Samia Haj Ahmed, Zohra Haouas, Amira Zarrouk, Gérard Lizard
    Abstract:

    Exposure of human neuronal SK-N-BE cells to Sodium Arsenate (AsV 0.1-400 μM; 48 h) induced a biphasic toxic effect evoking hormesis. Indeed, at low concentrations, AsV stimulates cell proliferation visualized by phase contrast microscopy, whereas at high concentrations, an induction of cell death associated with a loss of cell adhesion was observed. These side effects were confirmed with crystal violet test, cell cycle analysis, evaluation of the percentage of Ki67 positive cells, and staining with propidium iodide. The impact of AsV on mitochondrial functions, which was determined by the MTT assay, the measurement of mitochondrial transmembrane potential with DiOC6(3), and the rate of mitochondrial ATP, also support an hormesis process. In addition, in the presence of high concentrations of AsV, a significant decrease of the protein expression of OXPHOS complexes of the respiratory chain was observed by western blot supporting that AsV-induced cell death is associated with mitochondrial alterations. Therefore, there are some evidences of hormesis on AsV-treated SK-N-BE cells, and at high concentrations, the mitochondria are a target of toxicity induced by AsV.

  • Sodium Arsenate induce changes in fatty acids profiles and oxidative damage in kidney of rats
    Environmental Science and Pollution Research, 2014
    Co-Authors: Wafa Kharroubi, Mohamed Hammami, Zohra Haouas, Madiha Dhibi, Imed Chreif, Fadoua Neffati, Manel Mekni, Rachid Sakly
    Abstract:

    Six groups of rats (n = 10 per group) were exposed to 1 and 10 mg/l of Sodium Arsenate for 45 and 90 days. Kidneys from treated groups exposed to arsenic showed higher levels of trans isomers of oleic and linoleic acids as trans C181n-9, trans C18:1n-11, and trans C18:2n-6 isomers. However, a significant decrease in eicosenoic (C20:1n-9) and arachidonic (C20:4n-6) acids were observed in treated rats. Moreover, the “Δ5 desaturase index” and the saturated/polyunsaturated fatty acids ratio were increased. There was a significant increase in the level of malondialdehyde at 10 mg/l of treatment and in the amount of conjugated dienes after 90 days (p < 0.05). Significant kidney damage was observed at 10 mg/l by increase of plasma marker enzymes. Histological studies on the ultrastructure changes of kidney supported the toxic effect of Arsenate exposure. Arsenate intoxication activates significantly the superoxide dismutase at 10 mg/l for 90 days, whereas the catalase activity was markedly inhibited in all treated groups (p < 0.05). In addition, glutathione peroxidase activity was significantly increased at 45 days and dramatically declined after 90 days at 10 mg/l (p < 0.05). A significant increase in the level of glutathione was marked for the groups treated for 45 and 90 days at 1 mg/l followed by a significant decrease for rats exposed to 10 mg/l for 90 days. An increase in the level of protein carbonyl was observed in all treated groups (p < 0.05). In conclusion, the present study provides evidence for a direct effect of Arsenate on fatty acid (FA) metabolism which concerns the synthesis pathway of n-6 polyunsaturated fatty acids and leads to an increase in the trans FAs isomers. Therefore, FA-induced Arsenate kidney damage could contribute to trigger kidney cancer.

  • effects of Sodium Arsenate exposure on liver fatty acid profiles and oxidative stress in rats
    Environmental Science and Pollution Research, 2014
    Co-Authors: Wafa Kharroubi, Mohamed Hammami, Zohra Haouas, Madiha Dhibi, Imed Chreif, Fadoua Neffati, Rachid Sakly
    Abstract:

    The present study aimed to evaluate the effect of arsenic on liver fatty acids (FA) composition, hepatotoxicity and oxidative status markers in rats. Male rats were randomly devised to six groups (n = 10 per group) and exposed to Sodium Arsenate at a dose of 1 and 10 mg/l for 45 and 90 days. Arsenate exposure is associated with significant changes in the FA composition in liver. A significant increase of saturated fatty acids (SFA) in all treated groups (p < 0.01) and trans unsaturated fatty acids (trans UFA) in rats exposed both for short term for 10 mg/l (p < 0.05) and long term for 1 and 10 mg/l (p < 0.001) was observed. However, the cis UFA were significantly decreased in these groups (p < 0.05). A markedly increase of indicator in cell membrane viscosity expressed as SFA/UFA was reported in the treated groups (p < 0.001). A significant increase in the level of malondialdehyde by 38.3 % after 90 days of exposure at 10 mg/l was observed. Compared to control rats, significant liver damage was observed at 10 mg/l of Arsenate by increasing plasma marker enzymes after 90 days. It is through the histological investigations in hepatic tissues of exposed rats that these damage effects of Arsenate were confirmed. The antioxidant perturbations were observed to be more important at groups treated by the high dose (p < 0.05). An increase in the level of protein carbonyls was observed in all treated groups (p < 0.05). The present study provides evidence for a direct effect of arsenite on FA composition disturbance causing an increase of SFA and TFAs isomers, liver dysfunction and oxidative stress. Therefore, Arsenate can lead to hepatic damage and propensity towards liver cancer.

Gérard Lizard - One of the best experts on this subject based on the ideXlab platform.

  • Mitochondrial dysfunction, oxidative stress and apoptotic induction in microglial BV-2 cells treated with Sodium Arsenate.
    Journal of Environmental Sciences, 2017
    Co-Authors: Wafa Kharroubi, Samia Haj Ahmed, Thomas Nury, Pierre Andreoletti, Rachid Sakly, Mohamed Hammami, Gérard Lizard
    Abstract:

    The treatment of microglial BV-2 cells with Sodium Arsenate (As(V): 0.1-400μmol/L - 48hr) induces a dose-dependent response. The neurotoxic effects of high concentrations of As(V) (100, 200 and 400μmol/L) are characterized by increased levels of mitochondrial complexes I, II, and IV followed by increased superoxide anion generation. Moreover, As(V) triggers an apoptotic mode of cell death, demonstrated by an apoptotic SubG1 peak, associated with an alteration of plasma membrane integrity. There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP. It is therefore tempting to speculate that As(V) triggers mitochondrial dysfunction, which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage, which in turn induces an apoptotic mode of cell death.

  • Evidence of hormesis on human neuronal SK-N-BE cells treated with Sodium Arsenate: impact at the mitochondrial level.
    Environmental Science and Pollution Research, 2016
    Co-Authors: Wafa Kharroubi, Thomas Nury, Pierre Andreoletti, Rachid Sakly, Mohamed Hammami, Samia Haj Ahmed, Zohra Haouas, Amira Zarrouk, Gérard Lizard
    Abstract:

    Exposure of human neuronal SK-N-BE cells to Sodium Arsenate (AsV 0.1-400 μM; 48 h) induced a biphasic toxic effect evoking hormesis. Indeed, at low concentrations, AsV stimulates cell proliferation visualized by phase contrast microscopy, whereas at high concentrations, an induction of cell death associated with a loss of cell adhesion was observed. These side effects were confirmed with crystal violet test, cell cycle analysis, evaluation of the percentage of Ki67 positive cells, and staining with propidium iodide. The impact of AsV on mitochondrial functions, which was determined by the MTT assay, the measurement of mitochondrial transmembrane potential with DiOC6(3), and the rate of mitochondrial ATP, also support an hormesis process. In addition, in the presence of high concentrations of AsV, a significant decrease of the protein expression of OXPHOS complexes of the respiratory chain was observed by western blot supporting that AsV-induced cell death is associated with mitochondrial alterations. Therefore, there are some evidences of hormesis on AsV-treated SK-N-BE cells, and at high concentrations, the mitochondria are a target of toxicity induced by AsV.

  • differential alterations of lipid status and lipid metabolism induction of oxidative stress by Sodium Arsenate in female rat s liver and kidney
    Biomedical and Environmental Sciences, 2015
    Co-Authors: Kharroubi Wafa, Hammami Mohamed, Gérard Lizard, Dhibi Madiha, Chreif Imed, Sakly Rachid
    Abstract:

    Three groups of female rats ( n =6 per group) were exposed to 1 and 10 mg/L of Sodium Arsenate for 90 days. The antioxidant and peroxidation parameters in kidney and liver tissues were evaluated, also the fatty acid composition were determined. In liver the synthesis pathway of n-3 polyunsaturated fatty acids (PUFA) seemed to be more affected than the n-6 PUFA, while in kidney the n-6 pathway was more affected. The Δ5 ‘desaturase index’ was decreased in kidney. Both in liver and kidney an increase in the percentage of trans PUFA was observed, also we noted a disturbance in antioxidant parameters as SOD, GPx, CAT, and GSH ( P