The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform

Marcelo L Larramendy - One of the best experts on this subject based on the ideXlab platform.

  • the Chlorophenoxy Herbicide dicamba and its commercial formulation banvel induce genotoxicity and cytotoxicity in chinese hamster ovary cho cells
    Mutation Research-genetic Toxicology and Environmental Mutagenesis, 2007
    Co-Authors: Norma V González, Sonia Soloneski, Marcelo L Larramendy
    Abstract:

    The sister chromatid exchange (SCE) frequency, the cell-cycle progression analysis, and the single cell gel electrophoresis technique (SCGE, comet assay) were employed as genetic end-points to investigate the geno- and citotoxicity exerted by dicamba and one of its commercial formulation banvel (dicamba 57.71%) on Chinese hamster ovary (CHO) cells. Log-phase cells were treated with 1.0-500.0 microg/ml of the Herbicides and harvested 24 h later for SCE and cell-cycle progression analyses. All concentrations assessed of both test compounds induced higher SCE frequencies over control values. SCEs increased in a non-dose-dependent manner neither for the pure compound (r=0.48; P>0.05) nor for the commercial formulation (r=0.58, P>0.05). For the 200.0 microg/ml and 500.0 microg/ml dicamba doses and the 500.0 microg/ml banvel dose, a significant delay in the cell-cycle progression was found. A regression test showed that the proliferation rate index decreased as a function of either the concentration of dicamba (r=-0.98, P<0.05) or banvel (r=-0.88, P<0.01) titrated into cultures in the 1.0-500.0 microg/ml dose-range. SCGE performed on CHO cells after a 90 min pulse-treatment of dicamba and banvel within a 50.0-500.0 microg/ml dose-range revealed a clear increase in dicamba-induced DNA damage as an enhancement of the proportion of slightly damaged and damaged cells for all concentrations used (P<0.01); concomitantly, a decrease of undamaged cells was found over control values (P<0.01). In banvel-treated cells, a similar overall result was registered. Dicamba induced a significant increase both in comet length and width over control values (P<0.01) regardless of its concentration whereas banvel induced the same effect only within 100.0-500.0 microg/ml dose range (P<0.01). As detected by three highly sensitive bioassays, the present results clearly showed the capability of dicamba and banvel to induce DNA and cellular damage on CHO cells.

  • The Chlorophenoxy Herbicide dicamba and its commercial formulation banvel induce genotoxicity and cytotoxicity in Chinese hamster ovary (CHO) cells.
    Mutation research, 2007
    Co-Authors: Norma V González, Sonia Soloneski, Marcelo L Larramendy
    Abstract:

    The sister chromatid exchange (SCE) frequency, the cell-cycle progression analysis, and the single cell gel electrophoresis technique (SCGE, comet assay) were employed as genetic end-points to investigate the geno- and citotoxicity exerted by dicamba and one of its commercial formulation banvel (dicamba 57.71%) on Chinese hamster ovary (CHO) cells. Log-phase cells were treated with 1.0-500.0 microg/ml of the Herbicides and harvested 24 h later for SCE and cell-cycle progression analyses. All concentrations assessed of both test compounds induced higher SCE frequencies over control values. SCEs increased in a non-dose-dependent manner neither for the pure compound (r=0.48; P>0.05) nor for the commercial formulation (r=0.58, P>0.05). For the 200.0 microg/ml and 500.0 microg/ml dicamba doses and the 500.0 microg/ml banvel dose, a significant delay in the cell-cycle progression was found. A regression test showed that the proliferation rate index decreased as a function of either the concentration of dicamba (r=-0.98, P

Nicholas A Buckley - One of the best experts on this subject based on the ideXlab platform.

  • urinary alkalinisation for acute Chlorophenoxy Herbicide poisoning
    Cochrane Database of Systematic Reviews, 2007
    Co-Authors: Darren M Roberts, Nicholas A Buckley
    Abstract:

    Background Acute poisoning with Chlorophenoxy Herbicides (such as 2,4-D, MCPA, 2,4,5-T and mecoprop) is reported worldwide, potentially causing severe toxicity and death in exposed patients. Animal studies support the application of urinary alkalinisation (particularly using sodium bicarbonate) in the management of acute Chlorophenoxy Herbicide poisoning to facilitate excretion of these Herbicides. Some case reports of human exposure have suggested benefit from urinary alkalinisation also. Objectives To assess the efficacy of urinary alkalinisation, in particular sodium bicarbonate, for the treatment of acute Chlorophenoxy Herbicide poisoning. Search methods We searched MEDLINE, EMBASE, CENTRAL, Current Awareness in Clinical Toxicology, Info Trac, http://www.google.com.au, and Science Citation Index of studies identified by the previous searches. The bibliographies of identified articles were reviewed and experts in the field were contacted. Selection criteria Randomised controlled trials of urinary alkalinisation in patients ingesting a Chlorophenoxy Herbicide and presenting within 24 to 48 hours of poisoning were sought. The quality of studies and eligibility for inclusion was assessed using criteria by Jadad and Schulz. Data collection and analysis Authors independently extracted data from the identified studies using a pre-designed form. Study design, including the method of randomisation, participant characteristics, type of intervention and outcomes were all recorded. Main results No studies were identified which satisfied inclusion criteria. Authors' conclusions There is insufficient evidence to support the routine use of urinary alkalinisation for acute Chlorophenoxy Herbicide poisoning. A well conducted randomised controlled trial is urgently required to determine whether the efficacy and indications of this treatment.

  • The Cochrane Library - Urinary alkalinisation for acute Chlorophenoxy Herbicide poisoning
    The Cochrane database of systematic reviews, 2007
    Co-Authors: Darren M Roberts, Nicholas A Buckley
    Abstract:

    Background Acute poisoning with Chlorophenoxy Herbicides (such as 2,4-D, MCPA, 2,4,5-T and mecoprop) is reported worldwide, potentially causing severe toxicity and death in exposed patients. Animal studies support the application of urinary alkalinisation (particularly using sodium bicarbonate) in the management of acute Chlorophenoxy Herbicide poisoning to facilitate excretion of these Herbicides. Some case reports of human exposure have suggested benefit from urinary alkalinisation also. Objectives To assess the efficacy of urinary alkalinisation, in particular sodium bicarbonate, for the treatment of acute Chlorophenoxy Herbicide poisoning. Search methods We searched MEDLINE, EMBASE, CENTRAL, Current Awareness in Clinical Toxicology, Info Trac, http://www.google.com.au, and Science Citation Index of studies identified by the previous searches. The bibliographies of identified articles were reviewed and experts in the field were contacted. Selection criteria Randomised controlled trials of urinary alkalinisation in patients ingesting a Chlorophenoxy Herbicide and presenting within 24 to 48 hours of poisoning were sought. The quality of studies and eligibility for inclusion was assessed using criteria by Jadad and Schulz. Data collection and analysis Authors independently extracted data from the identified studies using a pre-designed form. Study design, including the method of randomisation, participant characteristics, type of intervention and outcomes were all recorded. Main results No studies were identified which satisfied inclusion criteria. Authors' conclusions There is insufficient evidence to support the routine use of urinary alkalinisation for acute Chlorophenoxy Herbicide poisoning. A well conducted randomised controlled trial is urgently required to determine whether the efficacy and indications of this treatment.

  • intentional self poisoning with the Chlorophenoxy Herbicide 4 chloro 2 methylphenoxyacetic acid mcpa
    Annals of Emergency Medicine, 2005
    Co-Authors: Darren M Roberts, Nicholas A Buckley, Ruwan Seneviratne, Fahim Mohammed, Renu Patel, Lalith Senarathna, Ariyasena Hittarage, Andrew H Dawson, Michael Eddleston
    Abstract:

    Study objective Data on poisoning with MCPA (4-chloro-2-methyl-phenoxyacetic acid) are limited to 6 case reports. Our objective is to describe outcomes from intentional self-poisoning with MCPA in a prospective case series of 181 patients presenting to hospitals in Sri Lanka. Methods Patient information was collected by on-site study physicians as part of an ongoing prospective cohort study of poisoned patients. Medical history, clinical details, and blood samples were obtained prospectively. Results Overall clinical toxicity was minimal in 85% of patients, including mild gastrointestinal symptoms in 44% of patients. More severe clinical signs of Chlorophenoxy poisoning reported previously, such as rhabdomyolysis, renal dysfunction, and coma, also occurred but were uncommon. Eight patients died (4.4%). Most deaths occurred suddenly from cardiorespiratory arrest within 48 hours of poisoning; the pathophysiological mechanism of death was not apparent. The correlation between admission plasma MCPA concentration and clinical markers of severity of toxicity (physical signs, symptoms, and increased creatine kinase level) was poor. Conclusion Intentional self-poisoning with MCPA generally causes mild toxicity, but cardiorespiratory arrest and death may occur. All patients should receive routine resuscitation and supportive care. It seems reasonable to correct acidosis and maintain an adequate urine output, but there is insufficient evidence to support other specific interventions. Our data do not support a clinical role for measurement of plasma MCPA in the acute management of poisoning, and insufficient data were available to fully examine the utility of measured electrolytes and creatine kinase levels.

Norma V González - One of the best experts on this subject based on the ideXlab platform.

  • the Chlorophenoxy Herbicide dicamba and its commercial formulation banvel induce genotoxicity and cytotoxicity in chinese hamster ovary cho cells
    Mutation Research-genetic Toxicology and Environmental Mutagenesis, 2007
    Co-Authors: Norma V González, Sonia Soloneski, Marcelo L Larramendy
    Abstract:

    The sister chromatid exchange (SCE) frequency, the cell-cycle progression analysis, and the single cell gel electrophoresis technique (SCGE, comet assay) were employed as genetic end-points to investigate the geno- and citotoxicity exerted by dicamba and one of its commercial formulation banvel (dicamba 57.71%) on Chinese hamster ovary (CHO) cells. Log-phase cells were treated with 1.0-500.0 microg/ml of the Herbicides and harvested 24 h later for SCE and cell-cycle progression analyses. All concentrations assessed of both test compounds induced higher SCE frequencies over control values. SCEs increased in a non-dose-dependent manner neither for the pure compound (r=0.48; P>0.05) nor for the commercial formulation (r=0.58, P>0.05). For the 200.0 microg/ml and 500.0 microg/ml dicamba doses and the 500.0 microg/ml banvel dose, a significant delay in the cell-cycle progression was found. A regression test showed that the proliferation rate index decreased as a function of either the concentration of dicamba (r=-0.98, P<0.05) or banvel (r=-0.88, P<0.01) titrated into cultures in the 1.0-500.0 microg/ml dose-range. SCGE performed on CHO cells after a 90 min pulse-treatment of dicamba and banvel within a 50.0-500.0 microg/ml dose-range revealed a clear increase in dicamba-induced DNA damage as an enhancement of the proportion of slightly damaged and damaged cells for all concentrations used (P<0.01); concomitantly, a decrease of undamaged cells was found over control values (P<0.01). In banvel-treated cells, a similar overall result was registered. Dicamba induced a significant increase both in comet length and width over control values (P<0.01) regardless of its concentration whereas banvel induced the same effect only within 100.0-500.0 microg/ml dose range (P<0.01). As detected by three highly sensitive bioassays, the present results clearly showed the capability of dicamba and banvel to induce DNA and cellular damage on CHO cells.

  • The Chlorophenoxy Herbicide dicamba and its commercial formulation banvel induce genotoxicity and cytotoxicity in Chinese hamster ovary (CHO) cells.
    Mutation research, 2007
    Co-Authors: Norma V González, Sonia Soloneski, Marcelo L Larramendy
    Abstract:

    The sister chromatid exchange (SCE) frequency, the cell-cycle progression analysis, and the single cell gel electrophoresis technique (SCGE, comet assay) were employed as genetic end-points to investigate the geno- and citotoxicity exerted by dicamba and one of its commercial formulation banvel (dicamba 57.71%) on Chinese hamster ovary (CHO) cells. Log-phase cells were treated with 1.0-500.0 microg/ml of the Herbicides and harvested 24 h later for SCE and cell-cycle progression analyses. All concentrations assessed of both test compounds induced higher SCE frequencies over control values. SCEs increased in a non-dose-dependent manner neither for the pure compound (r=0.48; P>0.05) nor for the commercial formulation (r=0.58, P>0.05). For the 200.0 microg/ml and 500.0 microg/ml dicamba doses and the 500.0 microg/ml banvel dose, a significant delay in the cell-cycle progression was found. A regression test showed that the proliferation rate index decreased as a function of either the concentration of dicamba (r=-0.98, P

Darren M Roberts - One of the best experts on this subject based on the ideXlab platform.

  • urinary alkalinisation for acute Chlorophenoxy Herbicide poisoning
    Cochrane Database of Systematic Reviews, 2007
    Co-Authors: Darren M Roberts, Nicholas A Buckley
    Abstract:

    Background Acute poisoning with Chlorophenoxy Herbicides (such as 2,4-D, MCPA, 2,4,5-T and mecoprop) is reported worldwide, potentially causing severe toxicity and death in exposed patients. Animal studies support the application of urinary alkalinisation (particularly using sodium bicarbonate) in the management of acute Chlorophenoxy Herbicide poisoning to facilitate excretion of these Herbicides. Some case reports of human exposure have suggested benefit from urinary alkalinisation also. Objectives To assess the efficacy of urinary alkalinisation, in particular sodium bicarbonate, for the treatment of acute Chlorophenoxy Herbicide poisoning. Search methods We searched MEDLINE, EMBASE, CENTRAL, Current Awareness in Clinical Toxicology, Info Trac, http://www.google.com.au, and Science Citation Index of studies identified by the previous searches. The bibliographies of identified articles were reviewed and experts in the field were contacted. Selection criteria Randomised controlled trials of urinary alkalinisation in patients ingesting a Chlorophenoxy Herbicide and presenting within 24 to 48 hours of poisoning were sought. The quality of studies and eligibility for inclusion was assessed using criteria by Jadad and Schulz. Data collection and analysis Authors independently extracted data from the identified studies using a pre-designed form. Study design, including the method of randomisation, participant characteristics, type of intervention and outcomes were all recorded. Main results No studies were identified which satisfied inclusion criteria. Authors' conclusions There is insufficient evidence to support the routine use of urinary alkalinisation for acute Chlorophenoxy Herbicide poisoning. A well conducted randomised controlled trial is urgently required to determine whether the efficacy and indications of this treatment.

  • The Cochrane Library - Urinary alkalinisation for acute Chlorophenoxy Herbicide poisoning
    The Cochrane database of systematic reviews, 2007
    Co-Authors: Darren M Roberts, Nicholas A Buckley
    Abstract:

    Background Acute poisoning with Chlorophenoxy Herbicides (such as 2,4-D, MCPA, 2,4,5-T and mecoprop) is reported worldwide, potentially causing severe toxicity and death in exposed patients. Animal studies support the application of urinary alkalinisation (particularly using sodium bicarbonate) in the management of acute Chlorophenoxy Herbicide poisoning to facilitate excretion of these Herbicides. Some case reports of human exposure have suggested benefit from urinary alkalinisation also. Objectives To assess the efficacy of urinary alkalinisation, in particular sodium bicarbonate, for the treatment of acute Chlorophenoxy Herbicide poisoning. Search methods We searched MEDLINE, EMBASE, CENTRAL, Current Awareness in Clinical Toxicology, Info Trac, http://www.google.com.au, and Science Citation Index of studies identified by the previous searches. The bibliographies of identified articles were reviewed and experts in the field were contacted. Selection criteria Randomised controlled trials of urinary alkalinisation in patients ingesting a Chlorophenoxy Herbicide and presenting within 24 to 48 hours of poisoning were sought. The quality of studies and eligibility for inclusion was assessed using criteria by Jadad and Schulz. Data collection and analysis Authors independently extracted data from the identified studies using a pre-designed form. Study design, including the method of randomisation, participant characteristics, type of intervention and outcomes were all recorded. Main results No studies were identified which satisfied inclusion criteria. Authors' conclusions There is insufficient evidence to support the routine use of urinary alkalinisation for acute Chlorophenoxy Herbicide poisoning. A well conducted randomised controlled trial is urgently required to determine whether the efficacy and indications of this treatment.

  • intentional self poisoning with the Chlorophenoxy Herbicide 4 chloro 2 methylphenoxyacetic acid mcpa
    Annals of Emergency Medicine, 2005
    Co-Authors: Darren M Roberts, Nicholas A Buckley, Ruwan Seneviratne, Fahim Mohammed, Renu Patel, Lalith Senarathna, Ariyasena Hittarage, Andrew H Dawson, Michael Eddleston
    Abstract:

    Study objective Data on poisoning with MCPA (4-chloro-2-methyl-phenoxyacetic acid) are limited to 6 case reports. Our objective is to describe outcomes from intentional self-poisoning with MCPA in a prospective case series of 181 patients presenting to hospitals in Sri Lanka. Methods Patient information was collected by on-site study physicians as part of an ongoing prospective cohort study of poisoned patients. Medical history, clinical details, and blood samples were obtained prospectively. Results Overall clinical toxicity was minimal in 85% of patients, including mild gastrointestinal symptoms in 44% of patients. More severe clinical signs of Chlorophenoxy poisoning reported previously, such as rhabdomyolysis, renal dysfunction, and coma, also occurred but were uncommon. Eight patients died (4.4%). Most deaths occurred suddenly from cardiorespiratory arrest within 48 hours of poisoning; the pathophysiological mechanism of death was not apparent. The correlation between admission plasma MCPA concentration and clinical markers of severity of toxicity (physical signs, symptoms, and increased creatine kinase level) was poor. Conclusion Intentional self-poisoning with MCPA generally causes mild toxicity, but cardiorespiratory arrest and death may occur. All patients should receive routine resuscitation and supportive care. It seems reasonable to correct acidosis and maintain an adequate urine output, but there is insufficient evidence to support other specific interventions. Our data do not support a clinical role for measurement of plasma MCPA in the acute management of poisoning, and insufficient data were available to fully examine the utility of measured electrolytes and creatine kinase levels.

Sonia Soloneski - One of the best experts on this subject based on the ideXlab platform.

  • the Chlorophenoxy Herbicide dicamba and its commercial formulation banvel induce genotoxicity and cytotoxicity in chinese hamster ovary cho cells
    Mutation Research-genetic Toxicology and Environmental Mutagenesis, 2007
    Co-Authors: Norma V González, Sonia Soloneski, Marcelo L Larramendy
    Abstract:

    The sister chromatid exchange (SCE) frequency, the cell-cycle progression analysis, and the single cell gel electrophoresis technique (SCGE, comet assay) were employed as genetic end-points to investigate the geno- and citotoxicity exerted by dicamba and one of its commercial formulation banvel (dicamba 57.71%) on Chinese hamster ovary (CHO) cells. Log-phase cells were treated with 1.0-500.0 microg/ml of the Herbicides and harvested 24 h later for SCE and cell-cycle progression analyses. All concentrations assessed of both test compounds induced higher SCE frequencies over control values. SCEs increased in a non-dose-dependent manner neither for the pure compound (r=0.48; P>0.05) nor for the commercial formulation (r=0.58, P>0.05). For the 200.0 microg/ml and 500.0 microg/ml dicamba doses and the 500.0 microg/ml banvel dose, a significant delay in the cell-cycle progression was found. A regression test showed that the proliferation rate index decreased as a function of either the concentration of dicamba (r=-0.98, P<0.05) or banvel (r=-0.88, P<0.01) titrated into cultures in the 1.0-500.0 microg/ml dose-range. SCGE performed on CHO cells after a 90 min pulse-treatment of dicamba and banvel within a 50.0-500.0 microg/ml dose-range revealed a clear increase in dicamba-induced DNA damage as an enhancement of the proportion of slightly damaged and damaged cells for all concentrations used (P<0.01); concomitantly, a decrease of undamaged cells was found over control values (P<0.01). In banvel-treated cells, a similar overall result was registered. Dicamba induced a significant increase both in comet length and width over control values (P<0.01) regardless of its concentration whereas banvel induced the same effect only within 100.0-500.0 microg/ml dose range (P<0.01). As detected by three highly sensitive bioassays, the present results clearly showed the capability of dicamba and banvel to induce DNA and cellular damage on CHO cells.

  • The Chlorophenoxy Herbicide dicamba and its commercial formulation banvel induce genotoxicity and cytotoxicity in Chinese hamster ovary (CHO) cells.
    Mutation research, 2007
    Co-Authors: Norma V González, Sonia Soloneski, Marcelo L Larramendy
    Abstract:

    The sister chromatid exchange (SCE) frequency, the cell-cycle progression analysis, and the single cell gel electrophoresis technique (SCGE, comet assay) were employed as genetic end-points to investigate the geno- and citotoxicity exerted by dicamba and one of its commercial formulation banvel (dicamba 57.71%) on Chinese hamster ovary (CHO) cells. Log-phase cells were treated with 1.0-500.0 microg/ml of the Herbicides and harvested 24 h later for SCE and cell-cycle progression analyses. All concentrations assessed of both test compounds induced higher SCE frequencies over control values. SCEs increased in a non-dose-dependent manner neither for the pure compound (r=0.48; P>0.05) nor for the commercial formulation (r=0.58, P>0.05). For the 200.0 microg/ml and 500.0 microg/ml dicamba doses and the 500.0 microg/ml banvel dose, a significant delay in the cell-cycle progression was found. A regression test showed that the proliferation rate index decreased as a function of either the concentration of dicamba (r=-0.98, P