Betaine protects cerebellum from oxidative stress following levodopa and benserazide administration in rats

Alirezaei, Masoud (2015) Betaine protects cerebellum from oxidative stress following levodopa and benserazide administration in rats. Iranian Journal of Basic Medical Sciences, 18 (10).


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Objective(s): The aim of the present study was to evaluate antioxidant and methyl donor effects of betaine in cerebellum following levodopa and benserazide administration in rats. Materials and Methods: Sprague‐Dawley male rats were treated with levodopa (LD), betaine (Bet), levodopa plus betaine (LD/Bet), levodopa plus benserazide (LD/Ben), levodopa plus betaine‐ benserazide (LD/Bet‐Ben), and the controls with vehicle for 10 consecutive days, orally. Results: Treatment of rats with LD and benserazide significantly increased total homocysteine in plasma of the LD/Ben group when compared to the other groups. Lipid peroxidation of cerebellum increased significantly in LD‐treated rats when compared to the other groups. In contrast, glutathione peroxidase activity and glutathione content in cerebellum were significantly higher in the betaine‐ treated rats when compared to the LD and LD/Ben groups. Serum dopamine concentration increased significantly in LD‐treated rats in comparison with the LD/Ben group. LD/Bet‐treated rats also demonstrated significantly higher dopamine levels when compared to the LD/Ben group. Conclusion: We observed valuable effects of Bet in combination with LD and benserazide, which routinely were used for Parkinson’s disease (PD) treatment, in experimentally‐induced oxidative stress and hyperhomocysteinemia in rats. Therefore, it seems that Bet is a vital and promising agent regarding PD for future clinical trials in humans. Article history: Received: Apr 9, 2014 Accepted: Jul 12, 2014 Keywords: Benserazide Betaine Cerebellum Homocysteine Levodopa Parkinson’s disease ►Please cite this article as: Alirezaei M. Betaine protects cerebellum from oxidative stress following levodopa and benserazide administration in rats. Iran J Basic Med Sci 2015; 18:950‐957. Introduction It is well known that oxidative stress plays a major role in the neurodegenerative process that underlies Parkinson’s disease (PD) (1, 2). Various experimental studies have also shown that levodopa (LD), the most effective dopaminergic agent for PD, may paradoxically contribute to neuronal damage through formation of free radicals and reactive oxygen species (ROS) (1, 3, 4). In this regard, a previous report indicated increased hydroxyl radical formation in blood cells of PD patients under treatment with LD when compared with both untreated PD patients and healthy subjects (5). Homocysteine (Hcy) is a neuro and vascular toxic sulfur‐containing intermediate product. Because the adverse effects of Hcy are most likely related to its prooxidant properties (6), a direct involvement of the amino acid in this phenomenon was hypothesized. Moreover, it has been shown that the elevated plasma Hcy levels found in PD patients treated with LD are associated with a nearly two‐fold increased prevalence of coronary artery diseases (7, 8). Previous reports also suggest that elevated plasma Hcy levels may be a risk factor for neuropsychiatric disorders such as stroke, dementia, depression, and PD (6, 8). Although the brain has defenses against ROS including dietary free radical scavengers (ascorbate, α‐tocopherol), the endogenous tripeptide glutathione (GSH), and antioxidant enzymes such as glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT), there is considerable evidence that oxidative damage directly or indirectly, due to free radical production and ROS, can lead to brain injury (6, 9). Hcy passes the blood‐brain‐ barrier (BBB) (10, 11), additional functional disturbance of the BBB leads to an unprotected exposure of the brain to Hcy. Hcy has various consequences for neural cells: oxidative stress, activation of caspases, mitochondrial dysfunction and increase of cytosolic calcium, which contribute to apoptosis (6, 12, 13). Hcy also inhibits the expression of antioxidant enzymes, which might potentiate the toxic effects of ROS (6, 14‐16). In *Corresponding author: Masoud Alirezaei. Division of Biochemistry, School of Veterinary Medicine, Lorestan University, Khorram Abad, Iran. Tel/Fax: +98‐ 661‐6200109; email: Archive

Item Type: Article
Subjects: R Medicine > R Medicine (General)
Depositing User: samira sepahvandy
Date Deposited: 21 Sep 2016 07:04
Last Modified: 21 Sep 2016 07:04

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