Volume 1, Issue 2 (2015)                   Pharm Biomed Res 2015, 1(2): 10-19 | Back to browse issues page


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1- Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
2- Faculty of Pharmacy and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran
3- Faculty of Advanced Sciences and Technology in Medicine, Tehran University of Medical Sciences, Tehran, Iran
4- Pharmacutical Science Research Center, Hemoglobinopathy Institute, Mazandaran University of Medical Sciences, Sari, Iran Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran
Abstract:   (5511 Views)

The objective of the present study was to investigate the role of nanocarrier of magnetic isotope of 25-Mg2+ (PMC16) in liver toxicity, ATP content and oxidative stress due to malathion (MAL) exposure. PMC16 nanoparticles were administered in different doses (0.05, 0.1 and 0.2 LD50) intravenously (iv) 40 minutes after a single MAL (0.25 LD50= 207 mg/kg) intraperitoneal (ip) injection as a complement to standard therapy of pralidoxime (PAM) and atropine (AT). MgSO4 was used as another supplement for comparison with PMC16. ATP/ADP ratio, antioxidant enzymes including catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and oxidative stress biomarker including lipid peroxidation (LPO) were evaluated in liver tissue cells. Results indicated that after MAL administration, ADP/ATP ratio had a significant increase in liver tissues in comparison with control but this ratio was improved using various doses of PMC16. LPO was significantly decreased at all doses of PMC16 and MgSO4 when compared with MAL-exposed group. SOD and CAT activities significantly were increased in MAL-treated group as compared to saline group. SOD was reduced by all doses of PMC16 and CAT activity was decreased in PMC16-0.1 group. These results lead us to conclude that PMC16 and MgSO4 are so useful for protection against MAL-induced liver toxicity, ATP depletion and oxidative damages.

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Type of Study: Original Research | Subject: Toxicology

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