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Role of Propolis on Oxidative Stress in Fish Brain

Authors :
Shapour Kakoolaki
Zeliha Selamoglu
Talas Oguz
Oguz Cakir
Osman Ciftci
Ilknur Ozdemir
Source :
Basic and Clinical Neuroscience, Vol 4, Iss 2, Pp 153-158 (2013)
Publication Year :
2013
Publisher :
Iran University of Medical Sciences, 2013.

Abstract

Introduction: Cypermethrin causes its neurotoxic effect through voltage-dependent sodium channels and integral protein ATPases in the neuronal membrane. Brain and nerve damage are often associated with low residual level of pesticides. In vitro and in vivo studies have also shown that pesticides cause free radical-mediated tissue damage in brain. Propolis has antioxidant properties. The main chemical classes found in propolis are flavonoids and phenolics. Bioflavonoids are antioxidant molecules that play important roles in scavenging free radicals, which are produced in neurodegenerative diseases and aging. Methods: To determine the protective role of propolis, rainbow trouts were treated with cypermethrin, followed by biochemical analyses of brain tissue. Fish were divided into four groups: control, propolis-treated, cypermethrin-treated, and cypermethrin+propolis-treated. Results: In fish brains, catalase (CAT) activity decreased (P≤0.001) and malondialdehyde (MDA) level increased (P≤0.001) in cypermethrin-treated group compared to control group. In cypermethrin + propolis-treated group CAT activity increased (P≤0.001) and MDA level decreased (P≤0.001) compared to cypermethrin group. Discussion: The results demonstrated that the negative effects, observed as a result of cypermethrin treatment, could be reversed by adding supplementary propolis. Propolis may improve some biochemical markers associated with oxidative stress in fish brain, after exposure to cypermethrin.

Details

Language :
English
ISSN :
2008126X and 22287442
Volume :
4
Issue :
2
Database :
Directory of Open Access Journals
Journal :
Basic and Clinical Neuroscience
Publication Type :
Academic Journal
Accession number :
edsdoj.86af6d44169c4592a71cef0a5fdde264
Document Type :
article