Logo-ajmb
Submitted: 19 Feb 2014
Revision: 07 Mar 2014
Accepted: 13 May 2014
ePublished: 25 Sep 2014
EndNote EndNote

(Enw Format - Win & Mac)

BibTeX BibTeX

(Bib Format - Win & Mac)

Bookends Bookends

(Ris Format - Mac only)

EasyBib EasyBib

(Ris Format - Win & Mac)

Medlars Medlars

(Txt Format - Win & Mac)

Mendeley Web Mendeley Web
Mendeley Mendeley

(Ris Format - Win & Mac)

Papers Papers

(Ris Format - Win & Mac)

ProCite ProCite

(Ris Format - Win & Mac)

Reference Manager Reference Manager

(Ris Format - Win only)

Refworks Refworks

(Refworks Format - Win & Mac)

Zotero Zotero

(Ris Format - Firefox Plugin)

Avicenna J Med Biochem. 2014;2(1): 2-18321.
doi: 10.17795/ajmb-18321
  Abstract View: 1798
  PDF Download: 975
  Full Text View: 1232

Research Article

Hepatoprotective Effects of Vitamin E Against Malathion-Induced Mitochondrial Dysfunction in Rat Liver

Akram Ranjbar 1*, Fariba Mohsenzadeh 2, Maryam Baeeri 3

1 Department of Toxicology and Pharmacology, Hamadan University of Medical Sciences, Hamadan, IR Iran
2 Department of Biology, Bu-Ali Sina University, Hamedan, IR Iran
3 Faculty of Pharmacy, Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, IR Iran
*Corresponding Author: *Corresponding author: Akram Ranjbar, Department of Toxicology and Pharmacology, Hamadan University of Medical Sciences, Hamadan, IR Iran. Tel/Fax: +98-8118380031, E-mail: , Email: akranjbar1389@yahoo.ccom

Abstract

Background: Malathion is an insecticide of the grouping of organophosphate pesticides (OPs), which shows strong insecticidal effects. In addition, vitamin E reacting to cell membrane site may prevent OP-induced oxidative injury.

Objectives: The aim of this study was to examine the protective function of vitamin E on toxicity of malathion, by measuring the activities of liver and liver mitochondrial superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (LPO), and glutathione peroxidase (GPx) in rats.

Materials and Methods: The mitochondrial viability was determined in liver. Effective doses of malathion (200 mg/kg/day) and vitamin E (alpha-tocopherylacetate [AT]; 15 mg/kg/day) were administered alone or in combination for 14 days. At the end of the experiment, the liver tissue and liver mitochondria of the animals were harvested and examined.

Results: In liver tissue, the activity of LPO and CAT was higher in the malathion group in comparison to controls. AT reduced malathion-induced LPO, SOD, CAT, and GPx in rat liver. Coadministration of AT with malathion improved LPO, SOD, and CAT levels in liver as well as CAT and GPx in liver mitochondria. Malathion-induced mitochondria toxicity was recovered by AT.

Conclusions: In conclusion, AT measurement can be beneficial for the safety or recovery of malathion-induced toxic injury in liver tissue and liver mitochondria.


Implication for health policy/practice/research/medical education:

 
This study proposed vitamin E as a new approach to the treatment of the oxidative damage caused by the organophosphorus poisoning, in which the antioxidants might prevent cellular damage. Results of the present study revealed that alpha-tocopheryl acetate normalizes oxidant/antioxidant balance in liver and therefore liver mitochondria is able to recover malathion-induced changes.

First Name
Last Name
Email Address
Comments
Security code


Abstract View: 1799

Your browser does not support the canvas element.


PDF Download: 975

Your browser does not support the canvas element.


Full Text View: 1232

Your browser does not support the canvas element.