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Assessment Role of Dehydroepiandrosterone (DHEA

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Assessment Role of Dehydroepiandrosterone (DHEA Asian Journal of Research in Medical and Pharmaceutical Sciences 3(3): 1-12, 2018; Article no.AJRIMPS.40465 ISSN: 2457-0745 Assessment Role of Dehydroepiandrosterone (DHEA) and Melatonin or Their Mixture on Physiological and Biochemical Parameters in Alzheimer's Rats Induced by Aluminium Chloride Mona, I. M. Shahin1* 1Department of Zoology, Women's College for Arts, Science and Education, Ain Shams University, Egypt. Author’s contribution The sole author designed, analyzed and interpreted and prepared the manuscript. Article Information DOI: 10.9734/AJRIMPS/2018/40465 Editor(s): (1) Anoja Priyadarshani Attanayake, Department of Biochemistry, Faculty of Medicine, University of Ruhuna, Sri Lanka. Reviewers: (1) Nina Filip, Grigore T. Popa University of Medicine and Pharmacy, Romania. (2) Tamer A. Gheita, Cairo University, Egypt. Complete Peer review History: http://www.sciencedomain.org/review-history/24679 Received 14th February 2018 Accepted 22nd April 2018 Original Research Article th Published 18 May 2018 ABSTRACT Alzheimer’s disease is progressing neuronal degeneration disease leads to impairment of memory and cognitive ability. It is the most common cause of dementia and its increases with age. the present study was to investigate whether the Dehydroepiandrosterone (DHEA) and Melatonin or their mixture could potentially prevent aluminium-induced neurotoxicity in the cerebral cortex, hippocampus and cerebellum of the rat brain. The results showed that malondialdehyde (MDA) and total nitric oxide (TNO) showed significant (P< 0.001) increase in the mean values of Al intoxicated rats. However, the cortex and hippocampus SOD, CAT activities and GSH contents were significantly decreased in rats intoxicated with AlCl3.Additionally, choline acetyl transferase ( ChAT ) was a significant increase. The administration of Dehydroepiandrosterone (DHEA) and Melatonin corrected all these alterations and the maximum ameliorating effects were exhibited in the rats treated with the mixture of Dehydroepiandrosterone (DHEA) and Melatonin. _____________________________________________________________________________________________________ *Corresponding author: E-mail: [email protected]; Shahin; AJRIMPS, 3(3): 1-12, 2018; Article no.AJRIMPS.40465 Keywords: Dehydroepiandrosterone; Melatonin; aluminium chloride; rats. 1. INTRODUCTION found in the elemental state; instead, it is found in oxides or silicates [3]. Despite the genetic and environmental factors and the ageing process itself, multiple evidence In nature, this trace element is found in its 3+ from experimental models and postmortem oxidized state Al (a soluble toxic form of Al), studies in Alzheimer’s disease (AD) brain tissue which binds to others molecules like chloride, demonstrate that neuro-degeneration is forming Aluminum chloride (AlCl3). Aluminium associated with morphological and biochemical chloride (AlCl3) is an important coagulant used in features. Considerable evidence suggests a role water treatment and purification being another for oxidative stress/damage (amyloid beta source ofe exposure. Two of the most common peptide, iron/hydrogen peroxide) or neurotoxic compounds are potassium aluminium sulfate 2 by-products of lipid peroxidation (4-hydroxy-2- (Kale(SO4) ·12H2O), and aluminium oxide nominal, acrolein) and inflammation, in the (Al2O3). Although aluminium is a widespread pathogenesis of neuron degeneration, which, in element, almost all metallic aluminium is turns, are known to cause cell death [1]. produced from the ore bauxite (AlOx(OH)3-2x). Bauxite is a complicated mixture of compounds Recently, several reports indicate that, among consisting of 55% of aluminium, oxygen, and factors, metal ions (Al, Zn, Cu, Fe, etc) could other elements [3]. specifically impair protein aggregation and their oligomeric toxicity. Also, metal-induced (direct) Abnormal production or clearance of a small and metal-amyloid-β (indirect) linked neuronal peptide, the amyloid β-peptide (Aβ), which is the cell death through the formation of reactive major constituent of the senile plaques, is a oxygen species (ROS) being critical to the widely accepted causative agent in degenerative understanding of the mechanisms which metal- disorders like an AD [4]. Aβ is a 39- to 43-residue induced cell death, and thus its role in peptide cleaved from the C-terminal region of a neurodegenerative disorders [2]. much larger protein, the amyloid precursor protein (APP), where the most abundant Some metals are essential for humans and for all fragments are Aβ (1–40) and Aβ (1–42), being forms of life. Even though metals are necessary the latter the most neurotoxic [4]. for biological systems, they are usually required only in trace amounts; in excess, it can be toxic, Several studies have shown that Aβ exerts its if not fatal. Environmental metal exposure has toxicity by generating reactive oxidative stress been suggested to be a risk factor for the AD. (ROS) molecules, leading to peroxidation of High-term exposure to certain metals like membrane lipids and lipoproteins, induction of manganese (Mn), iron (Fe), aluminum (Al) and H2O2 and hydroxynonenal (HNE) in neurons, many others like copper (Cu), mercury (Hg), zinc damages DNA and transport enzymes (Zn), lead (Pb), arsenic (As), alone or in inactivation [5]. In addition to a high metabolically combination, can increase neurodegenerative levels of ROS, there are other sources that are process, especially to Alzheimer’s disease (AD). thought to play an important role in the AD Aluminium (Al) is the most widely distributed progression. Among them, mitochondrial and metal in the environment and is extensively used metal abnormalities are the major sources of in a wide variety of products: cans, foils and oxidative stress [6]. There is some experimental kitchen utensils, as well as parts of evidence that Al exposure can adversely affect aeroplanes, rockets and other items that the dopaminergic system. Extended exposure to require a strong, light material. It can be 100 mM Al lactate increased striatal levels of the deposited on the surface of the glass to make dopamine metabolite, what, in turns, suggests mirrors and also to make synthetic rubies that exposure to Al may cause an increased and sapphires for lasers. Aluminium (Al) is turnover of dopamine [7]. found in the environment in its natural forms or as a source of human contamination Being involved in the production of reactive resulting from mining and smelting, activities that oxygen species (ROS), aluminium may cause increase their distribution throughout the impairments in mitochondrial bioenergetics and environment. Al occurs naturally only in may lead to the generation of oxidative stress compounds, never as a pure metal. Because of which may lead to a gradual accumulation of its strong affinity to oxygen, it is almost never oxidatively modified cellular proteins, lipids and 2 Shahin; AJRIMPS, 3(3): 1-12, 2018; Article no.AJRIMPS.40465 affects endogenous antioxidant enzyme activity, In the other experiment, five comparisons were leading to degeneration of neuronal cells. In this done between normal control rats (n= 10 rats) way, aluminium is a strong candidate for and four groups of rats administration aluminium consideration as a subtle promoter of events chloride. The first experimentally functional typically associated with brain ageing and neurotoxicity group was served as recovery neurodegenerative disorders [8]. The present group. The second functional neurotoxicity study aimed to investigate the role of oxidative group rats were treated with oro-gastric stress and the status of the antioxidant system in tube which dissolved in 5% DMSO in saline the management of aluminium chloride (AlCl3) at a dose of 250 mg DHEA/Kg b.w./day for induced brain toxicity in rats and further to one month [11]. The third functional elucidate the potential role of neurotoxicity group rats were treated orally Dehydroepiandrosterone (DHEA) and Melatonin with 7 mg melatonin /kg b.w./days which or their mixture in alleviating such negative dissolved in 5% DMSO in the aid of oro-gastric effects. tube for one month according to Esparza et al. [12] and stated with Sushma et al. [13]. 2. MATERIALS AND METHODS The fourth functional neurotoxicity group rat as received both melatonin and DHEA for 2.1 Animals the same previous period. All animal groups were divided into two intervals (2 & 4 weeks and Sixty male albino rats (Sprague Dawley), five rats in each group). weighing 225±10 and obtained from The Nile Co. for Pharmaceuticals and Chemical Industries, At the end of each experimental, rats were Cairo, Egypt were used. They were still in sacrificed 24 h after the last test and the stainless cages, two to three per cage, at a brain tissues were dissected and washed temperature of 25±1°C with alternatively 12 with ice-cold saline. The brain tissues were hour light and dark cycles. Water was given either subjected to biochemical analysis for rats ad-libitum and they were kept under immediately or kept frozen at -80°C until the the same controlled conditions and provided time of analysis where they were homogenized with their daily dietary requirements of standard in saline. The brain tissue homogenates diet pellets according to NRC [9] contained were used to measure oxidative/antioxidant 20% protein, 5% fibre, 3.5% fat, 6.5% ash and profile; lipid peroxides expressed as a vitamin mixture. The study was conducted malondialdehyde (MDA) and total nitric oxide in accordance with the ethical guidelines of (TNO)
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