Abstract
Effects of ROS generation have been postulated to be major contributors to lead-exposure related disease. The aim of the study was to investigate the effect of aqueous extract of wormwood (Artemisia absinthium) on oxidative stress in rats protractedly exposed to lead. Aqueous extract of wormwood plant was administered orally (200 mg x kg(-1) body weight). Plasma vitamin C, E and non-protein thiol concentrations, red blood cells (RBC) thiobarbituric acid reactive substances, reduced glutathione levels and haemolysis test were evaluated. In addition, RBC antioxidant enzymes activities such as superoxide dismutases, catalase, glutathione peroxidase, glutathione reductase were also estimated. After 11-weeks, significant decreases of plasma vitamin C, E, non protein-thiol (NP-SH) and RBC-reduced glutathione levels were observed in Pb compared to control group (-32.9%, -57.1%, -53.1%, -33.9%, respectively); superoxide dismutase, glutathione peroxidase, uric aminolevulinic acid and haemolysis test significantly increased in Pb compared to control group (+64.3%, +40.3%, +145%, +44.3%, respectively). In our investigation, after 4-weeks of treatment all treated groups did not show any difference compared to the control group, except for glutathione peroxidase and RBC-superoxide dismutase activity (-15.7% and +16.4%, respectively). The findings of this study suggest that wormwood (Artemisia absinthium) extract restored the enzymes activities perturbed by exposure to lead, and had a protective role against lipid peroxidation.
Highlights
The toxicokinetics of lead is a complex process (Leggett, 1993; Cory-Schlecta and Schaumburg, 2000)
Significant difference in blood and urine lead concentration was observed between lead acetate (Pb) group at 11-weeks of intoxication compared to Pb/Abs and Pb/water groups (Table.1)
The levels of uric δ-aminolevulinic were significantly lower in control vs. Pb groups and the Pb/water groups; the values of uric δ-aminolevulinic are significativelly decreased in Pb/Abs group the Pb group (-54.74%)
Summary
The toxicokinetics of lead is a complex process (Leggett, 1993; Cory-Schlecta and Schaumburg, 2000). Absorbed lead is carried in the blood circulation, wherein the major burden (95%) is on the erythrocytes and partly to other tissues-in the plasma. In addition to killing cells via excitotoxicity and apoptosis, lead causes toxic effects by oxidative stress either directly or by indirectly-produced lipid peroxidation. Enhances lipid peroxidation and decreases cell membrane fluidity of developing rats (Gurer and Ercal; 2000; Villeda-Hernandez et al, 2001). To membrane peroxidation, lead exposure causes haemoglobin oxidation, which can cause RBC haemolysis. As a result, elevated levels of the substrate ALA are found in both the blood and urine of lead-exposed subjects (Farant and Wigfield; 1982). Elevated levels of ALA generate hydrogen peroxide (H2O2) and superoxide radical (O2-), and interact with oxyhemoglobin, resulting in the generation of hydroxyl radicals (OH), the most reactive of the free radicals (Bechara, 1996; Courtois et al, 2003)
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