Paper Information

Title: 

OXIDATIVE STRESS IN RAT BRAIN FOLLOWING EXPOSURE TO PARAOXON

Type: POSTER
Author(s): GHANI E.*,JAFARI M.,MOHAMMADI M.,GHASEMI A.,MAHDAVINASAB H.,KHOUSHBATEN A.,ASGARI A.R.
 
 *DEPARTEMENT OF PHYSIOLOGY AND BIOPHYSICS, SCHOOL OF MEDICINE, BAQIYATALLAH UNIVERSITY OF MEDICAL SCIENCE
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: The acute toxicity effect of OP is due to the inhibition of acetylcholinesterase (AChE), which occurs in the central nervous system of most animals, including humans. Investigations show that different classes of pesticides, including OPs, may induce in vitro and in vivo generation of reactive oxygen species (ROS). In physiological conditions, a balance exists between production and elimination of ROS. The purpose of this study was to evaluate post exposure oxidative stress in the brain of rat due to paraoxon.
Methods: Male Wistar rats (200-250g) were randomly divided into five groups including: control, sham (corn oil), and three groups receiving different doses (0.1LD50, 0.5LD50, LD50) of paraoxon (ip injection). Four hours after injection, animals were anesthetized by ether and were decapitated. The brain was quickly removed and transferred to liquid nitrogen.
Results: Paraoxon, dose dependently, induced AChE inhibition. Furthermore, paraoxon increased the activity of superoxide dismutase, catalase and decreased the level of glutathione. malondialdehyde concentration didn't change following paraoxon intoxication.
Conclusion: present study shows that paraoxon induces elevation in the production of free radicals and oxidative stress. Elevation of catalase and superoxide dismutase activity and reduction in the level of glutathione indicate that first line of body defense is activated.

 
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