<abstract xml:lang="en" xmlns="http://www.w3.org/1999/xhtml"><p>The aim of this study was to investigate the effect of clomazone herbicide on oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes in <italic>in vitro</italic> conditions. The activity of catalase (CAT), superoxide dismutase (SOD) and acetylcholinesterase (AChE), as well as the levels of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) were measured in human erythrocytes exposed (<italic>in vitro</italic>) to clomazone at varying concentrations in the range of 0, 100, 250 and 500 μg/L for 1 h at 37°C. TBARS levels were significantly higher in erythrocytes incubated with clomazone at 100, 250 and 500 μg/L. However, erythrocyte CAT and AChE activities were decreased at all concentrations tested. SOD activity was increased only at 100 μg/L of clomazone. GSH levels did not change with clomazone exposure. These results clearly showed clomazone to induce oxidative stress and AChE inhibition in human erythrocytes (<italic>in vitro</italic>). We, thus, suggest a possible role of ROS on toxicity mechanism induced by clomazone in humans.</p></abstract>

The aim of this study was to investigate the effect of clomazone herbicide on oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes in in vitro conditions. The activity of catalase (CAT), superoxide dismutase (SOD) and acetylcholinesterase (AChE), as well as the levels of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) were measured in human erythrocytes exposed (in vitro) to clomazone at varying concentrations in the range of 0, 100, 250 and 500 μg/L for 1 h at 37°C. TBARS levels were significantly higher in erythrocytes incubated with clomazone at 100, 250 and 500 μg/L. However, erythrocyte CAT and AChE activities were decreased at all concentrations tested. SOD activity was increased only at 100 μg/L of clomazone. GSH levels did not change with clomazone exposure. These results clearly showed clomazone to induce oxidative stress and AChE inhibition in human erythrocytes (in vitro). We, thus, suggest a possible role of ROS on toxicity mechanism induced by clomazone in humans.

Oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes exposed to clomazone (<italic>in vitro</italic>)

Departamento de Química, Centro de Ciências Naturais e Exatas, Programa de Pós-Graduação em Bioquímica Toxicológica, Universidade Federal de Santa Maria, RS, Brazil

Interdisciplinary Toxicology

Oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes exposed to clomazone ()

The aim of this study was to investigate the effect of clomazone herbicide on oxidative stress biomarkers and acetylcholinesterase activity in human...

Oxidative stress biomarkers and acetylcholinesterase activity in human erythrocytes exposed to clomazone (in vitro)

Online veröffentlicht: 24. Okt. 2011

Seitenbereich: 149 - 153

DOI: https://doi.org/10.2478/v10102-011-0023-9

Schlüsselwörter
clomazone, erythrocytes, oxidative stress, acetylcholinesterase

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