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.

Highlights

  • The widespread use of pesticides in agriculture results in continuous exposure of human populations

  • 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

  • Considering the fact that erythrocytes are susceptible to oxidative stress induced by pesticide as well as that studies describing the role of reactive oxygen species (ROS) in clomazone toxicity are limited, the aim of this study was to investigate the effect of clomazone on oxidative stress biomarkers and AChE activity in human erythrocytes

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Summary

Introduction

The widespread use of pesticides in agriculture results in continuous exposure of human populations. Low-level exposure to pesticides is known to produce a variety of biochemical changes such as target cell/receptor binding, protein and DNA adduct formation, as well as induction or inhibition of enzymes (López et al, 2007). Biochemical and physiological functions of red blood cells (RBC) can be affected by pesticides. Erythrocytes are sensitive to oxidative damage due to the presence of high polyunsaturated fatty acid content in their membranes and high cellular concentrations of oxygen and haemoglobin (Hgb) (Prasanthi et al, 2005; Mansour & Mossa, 2009). It is speculated that oxidative stress in erythrocytes may lead to significant alterations in their structural conformation, which may compromise effective blood flow, oxygen uptake and release (Prasanthi et al, 2005). LPO, in particular, has been suggested to be one of the mechanisms of pesticide-induced toxicity (Mansour & Mossa, 2009)

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