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J Food Sci Technol. 2016 Mar;53(3):1454-64. doi: 10.1007/s13197-015-2150-3. Epub 2016 Jan 5.

Extra virgin olive oil modulates brain docosahexaenoic acid level and oxidative damage caused by 2,4-Dichlorophenoxyacetic acid in rats.

Author information

1
Biochemistry Laboratory, LR12ES05 "Nutrition-Functional Foods & Vascular Health", Faculty of Medicine, University of Monastir, Monastir, Tunisia.
2
Laboratory of Histology and Cytogenetic, UR02/08-03, Faculty of Medicine, University of Monastir, Monastir, Tunisia.

Abstract

Oxidative stress is an important pathomechanism of neurological disorders such as Alzheimer disease and Parkinson disease, cardiovascular disorders and many others. This study sought to verify whether extra-virgin olive oil (EVOO), lipophilic fraction (OOLF) and hydrophilic fraction (OOHF) exerted a brain protective effect against the oxidative stress caused by 2,4-dichlorophenoxyacetic acid (2,4-D) pesticide at a dose of 5 mg/kg body weight. 2,4-D, EVOO and its fractions were administered to rats by gavages for four consecutive weeks. Oxidative stress was assessed by measuring brain lipid peroxide level, acetylcholinesterase (AChE), antioxidant enzyme activities and fatty acid composition. 2,4-D induced a decrease in both plasma and brain acetylcholinesterase activity and a rise in Brain TBARS (Thiobarbituric acid reactive substances) level and antioxidant enzyme activities compared with the control group. These changes were partly reversed by either EVOO or its fractions oral administration to 2,4-D treated rats. EVOO enhanced a neuroprotective effect evaluated by the restoration of brain fatty acid composition especially the level of docosahexaenoic acid (DHA). Our results indicate that EVOO exerts a neuroprotective activity against oxidative damage in brain induced by 2,4-D, which could be attributed to its antioxidative property.

KEYWORDS:

Acetylcholinesterase; Brain and 2,4-D; Extra virgin olive oil; Oxidative stress; Rat

PMID:
27570270
PMCID:
PMC4984713
[Available on 2017-03-01]
DOI:
10.1007/s13197-015-2150-3

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