Levocarnitine Improves AlCl3-Induced Spatial Working Memory Impairment in Swiss albino Mice.

Md Mamun Al-Amin,Md Ashraful Alam,Murad Hossain,Preeti Jain,Mohsin Kazi,Hasan Mahmud Reza,Mohammad Raish,Mohammed Nazmul Alam,Abdulmohsen Alqahtani,Ajaz Ahmad,Md Irfan Amin Chowdury,A R M Saifullah

doi:10.3389/fnins.2019.00278

Md Mamun Al-Amin, Md Ashraful Alam + Show 10 more

Open Access

https://doi.org/10.3389/fnins.2019.00278

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Abstract

Background: Aluminum, a neurotoxic substance, causes oxidative stress induced-neurodegenerative diseases. Several lines of evidence suggest that levocarnitine has an antioxidant effect and also plays an important role in beta-oxidation of fatty acids. However, the role of levocarnitine in aluminum-induced neurotoxicity has not been well documented. Here we aimed to investigate the effect of levocarnitine on aluminum chloride (AlCl3)-induced oxidative stress and memory dysfunction.Methods: Male Swiss albino mice (n = 30) were treated with either control (saline) or AlCl3 or AlCl3 plus levocarnitine or levocarnitine or astaxanthin plus AlCl3 or astaxanthin alone. The spatial working memory was determined by radial arm maze (RAM). In addition, we measured the lipid peroxidation (MDA), glutathione (GSH), advanced oxidation of protein products (AOPP), nitric oxide (NO) and activity of superoxide dismutase (SOD) in the various brain regions including prefrontal cortex (PFC), striatum (ST), parietal cortex (PC), hippocampus (HIP) hypothalamus (HT) and cerebellum (CB). We used astaxanthin as a standard antioxidant to compare the antioxidant activity of levocarnitine.Results: The RAM data showed that AlCl3 treatment (50 mg/kg) for 2 weeks resulted in a significant deficit in spatial learning in mice. Moreover, aluminum exposure significantly (p < 0.05) increased the level of oxidative stress markers such as MDA, GSH, AOPP and NO in the various brain regions compared to the controls. In addition, combined administration of levocarnitine and AlCl3 significantly (p < 0.05) lowered the MDA, AOPP, GSH and NO levels in mice.Conclusion: Our results demonstrate that levocarnitine could serve as a potential therapeutic agent in the treatment of oxidative stress associated diseases as well as in memory impairment.

Highlights

MATERIALS AND METHODSHomeostasis of metal ions is highly important for normal cognitive function
Aluminum exposure significantly (p < 0.05) increased the level of oxidative stress markers such as measured the lipid peroxidation (MDA), GSH, Advanced Oxidation of Protein Products (AOPP) and Nitric Oxide (NO) in the various brain regions compared to the controls
The results of this radial arm maze (RAM) test suggest that levocarnitine intake may facilitate the finding of the target, suggesting an improvement of the spatial working memory performance

Summary

Introduction

MATERIALS AND METHODSHomeostasis of metal ions is highly important for normal cognitive function. Aluminum has been shown to cause oxidative stress (OS)-induced neurodegeneration through iron accumulation and reactive oxygen species (ROS) formation (Wu et al, 2012). ROS alters the level of antioxidant enzymes such as catalase (CAT) and superoxide dismutase (SOD), and it was reported that the activity of SOD decreased in the hippocampus and cerebral cortex of the brain in response to the oxidative stress (Sitta et al, 2009). A neurotoxic substance, causes oxidative stress inducedneurodegenerative diseases. Several lines of evidence suggest that levocarnitine has an antioxidant effect and plays an important role in beta-oxidation of fatty acids. The role of levocarnitine in aluminum-induced neurotoxicity has not been well documented. We aimed to investigate the effect of levocarnitine on aluminum chloride (AlCl3)-induced oxidative stress and memory dysfunction

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