Biochemicaleffect of Honey as an Anti-Oxidant in the treatment of the Childhood Refractory Epilepsy

Abstract

Epilepsy affects approximately 50 million people worldwide and is defined as a chronic disorder of the brain that is characterized by spontaneous and recurrent seizure activity, which is triggered by the abnormal discharge of neurons (Kramer and Cash, 2012). Treatment of this neurological disorder deserves special attention. Although anticonvulsant drugs have proven their efficacy, their use has demonstrated considerable side-effects. Furthermore, patients suffer from intractable conditions related to the type of crisis, drug resistance or other factors. Thus, there is a need for the development of new alternative therapeutic tools (Lopes et al., 2013). Honey is a supersaturated solution of sugars, which contains more than 180 other constituents like enzymes, amino acids and organic acids, carotenoids, Maillard reaction products, vitamins, minerals and polyphenols (Gheldorf et al., 2002). The minor compounds give the bioactive properties of honey, such as phenols (flavonoids and phenolic acids), and some studies have indicated that these are more potent regarding the antioxidant effect than vitamin C or E (Beretta et al., 2005). Honey is known to be rich in enzymatic and non-enzymatic antioxidants, including glucose-oxidase, catalase, flavonoids, ascorbic acid, phenolic acids and carotenoids (Batrušaityte˙ et al., 2007). Naturally, honey has been traditionally recognized as a valuable source of energy. It has also been recognized for its antimicrobial and antioxidant characteristics (Alvarez-Suarez et al., 2010). Therefore, honey has attracted attention in recent years as a useful or potential substance used in medicine and cosmetics products. The chemical composition of propolis is quite complicated. More than 300 compounds such as polyphenols, phenolic aldehydes, sequiterpene quinines, coumarins, amino acids, steroids and inorganic compounds have been identified in propolis samples (Khalil, 2006). Oxidative stress is regarded as possible mechanisms in the pathogenesis of epilepsy. Studies have already verified that status epilepticus changes redox potential and decreases the level of ATP, which can lead to a collapse in brain energy production and supply. Liang and Patel have demonstrated oxidative damage to susceptible targets (protein, lipids, and DNA) caused by persistent seizures (status epilepticus) (Liang and Patel, 2006). Several studies (animal models and genetic studies) have demonstrated an increase in mitochondrial O&NS and subsequent cell damage after persistent seizures (Chuang, 2010). Antioxidants are endogenous or exogenous compounds that either reduce the formation of free radicals or react with and neutralize them, thus potentially protecting the cell from oxidative injury. Because the biochemistry of free radical injury is complex, many substances may act as potential antioxidants and thus provide protection against disease or limit its consequences (Hamid et al., 2010). The main purpose of this study was to assess the efficacy honey as antioxidant in children with refractory epilepsy. This study was carried as prospective randomized controlled study including 32 epileptic patients with refractory epilepsy recruited among those who attending to pediatric neurology clinic, Ain Shams University children Hospitals, Cairo, Egypt. The patients had beenrandomized into two parallel groups (computer randomization); group 1(included 20 patients) received honey at a dose (2ml/kg/dose twice weekly) for eight weeks and group 2 (included 12 patients) received placebo (molasses) for eight weeks at the same dose. Honey dissolved in tape water in a dose 1: 4 and was given before meal.