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In Vitro Protection of Human Lymphocytes From Toxic Effects of Chlorpyrifos by Selenium-Enriched Medicines



Navaeinigjeh M1, 2 ; Asadi H3 ; Baeeri M1 ; Pedram S3 ; Rezvanfar MA1 ; Mohammadirad A1 ; Abdollahi M1, 3
Authors
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Authors Affiliations
  1. 1. Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Tissue Engineering, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Toxicology and Poisoning Research Center, Department of Toxicology and Pharmacology, Tehran University of Medical Sciences, Tehran, Iran

Source: Iranian Journal of Basic Medical Sciences Published:2015

Abstract

Objective(s): Chlorpyrifos (CP) is a broad-spectrum organophosphorus pesticide used extensively in agricultural and domestic pest control, accounting for 50% of the global insecticidal use. In the present study, protective effects of two selenium-enriched strong antioxidative medicines IMOD and Angipars were examined in human lymphocytes treated with CP in vitro. Materials and Methods: Isolated lymphocytes were exposed to 12 μg/ml CP either alone or in combination with effective doses (ED50) of IMOD (0.2 μg/ml) and Angipars (1 μg/ml). After 3 days incubation, the viability and oxidative stress markers including cellular lipid peroxidation (LPO), myeloperoxidase (MPO), total thiol molecules (TTM), and total antioxidant power (TAP) were evaluated. Also, the levels of tumor necrosis factor-α (TNF-α), as inflammatory index along with acetylcholinesterase (AChE) activity and cell apoptosis were assessed by flow cytometry. Results: Results indicated that effective doses of IMOD and Angipars reduced CP-exposed lymphocyte mortality rate along with oxidative stress. Both agents restored CP-induced elevation of TNF-α and protected the lymphocytes from CP-induced apoptosis and necrosis. Conclusion: Overall, results confirm that IMOD and Angipars reduce the toxic effects associated with CP through free radical scavenging and protection from apoptosis and necrosis. © 2015, Mashhad University of Medical Sciences. All rights reserved.
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