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BioMed Research International
Volume 2013 (2013), Article ID 859085, 11 pages
Research Article

Amelioration of Prallethrin-Induced Oxidative Stress and Hepatotoxicity in Rat by the Administration of Origanum majorana Essential Oil

1Environmental Toxicology Research Unit (ETRU), Pesticide Chemistry Department, National Research Centre (NRC), Tahrir Street, Dokki, Giza, Egypt
2Department of Biochemistry, National Research Centre (NRC), Tahrir Street, Dokki, Giza, Egypt
3Université de Toulouse, Faculté de Pharmacie de Toulouse, Université Paul-Sabatier, Laboratoire des IMRCP-UMR CNRS-UPS 5623, Cedex 9, 31062 Toulouse, France

Received 18 July 2013; Revised 1 November 2013; Accepted 1 November 2013

Academic Editor: Robert J. Lee

Copyright © 2013 Abdel-Tawab H. Mossa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This study was carried out to evaluate the adverse effects of exposure to prallethrin on oxidant/antioxidant status and liver dysfunction biomarkers and the protective role of Origanum majorana essential oil (EO) in rat. Male rats were divided into 4 groups: (i) received only olive oil (ii) treated with 64.0 mg/kg body weight prallethrin (1/10 LD50) in olive oil via oral route daily for 28 days, (iii) treated with 64.0 mg/kg body weight prallethrin (1/10 LD50) and EO (160 μL/kg b.wt.) in olive oil and (iv) received EO (160 μL/kg b.wt.) in olive oil via oral route twice daily for 28 days. Prallethrin treatment caused decrease in body weight gain and increase in relative liver weight. There was a significant increase in the activity of serum marker enzymes, aspartate transaminase, alanine transaminase, and alkaline phosphatase. It caused increase in thiobarbituric acid reactive substances and reduction in the activities of superoxide dismutase, catalase, and glutathione-S-transferase in liver. Consistent histological changes were found in the liver of prallethrin treatment. EO showed significant protection with the depletion of serum marker enzymes and replenishment of antioxidant status and brought all the values to near normal, indicating the protective effect of EO. We can conclude that prallethrin caused oxidative damage and liver injury in male rat and co-administration of EO attenuated the toxic effect of prallethrin. These results demonstrate that administration of EO may be useful, easy, and economical to protect human against pyrethroids toxic effects.