Protective Role ofFicus caricaStem Extract against Hepatic Oxidative Damage Induced by Methanol in Male Wistar Rats

Mongi Saoudi,Abdelfattah El Feki

doi:10.1155/2012/150458

Abstract

The present study was aimed to investigate the antioxidant activity of Ficus carica stem extract (FE) in methanol-induced hepatotoxicity in male Wistar rats. The rats were divided into two batches: 16 control rats (C) drinking tap water and 16 treated rats drinking Ficus carica stem extract for six weeks. Then, each group was divided into two subgroups, and one of them was intraperitoneally injected (i.p.) daily methanol at a dose of 2.37 g/kg body weight i.p. for 30 days, for four weeks. The results showed that FE was found to contain large amounts of polyphenols and carotenoids. The treatment with methanol exhibited a significant increase of serum hepatic biochemical parameters (ALT, AST, ALP, and LDH) and hepatic lipid peroxidation. Hepatic antioxidant enzymes, namely, SOD, CAT, and GSH-Px, were significantly decreased in methanol-treated animals. FE treatment prior to methanol intoxication has significant role in protecting animals from methanol-induced hepatic oxidative damage.

Highlights

Methanol, known as methyl alcohol and wood alcohol, is a primary alcohol with the chemical formula CH3OH
The F. carica stem extract contained phenolic compounds (133 ± 3.50 mg GAE/g), in which its level was expressed as gallic acid equivalents
Previous works demonstrated that F. carica was chosen for its abundance of phenols, essential oils, and flavonoids, which are effective on bacteria through compounds produced such as resveratrol, psoralen, and bergapten

Summary

Introduction

Known as methyl alcohol and wood alcohol, is a primary alcohol with the chemical formula CH3OH. It is a highly toxic alcohol commonly found in automobile windshield washer solvent, gas line antifreeze, copy machine fluid, fuel for small stoves, and paint strippers and used as industrial solvent. The simplest of all alcohols, is toxic to humans. The methanol could initiate ROS formation directly via a free radical intermediate, or possibly indirectly through mechanisms like the activation and/or enhancement of ROSproducing NADPH oxidases, which has been reported for ethanol [1]. It is associated with mitochondrial damage and increased microsomal proliferation resulting in increased production of oxygen radicals [2]

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