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Betaine as a methyl donor and an antioxidant agent in levodopa-induced hyperhomocysteinemia and oxidative stress in rat's kidney
2014
Alirezaei, Masoud
BACKGROUND: Betaine has been shown to be antioxidantand methyl donor effects in our recent studies. OBJECTIVES: Inthe present study, the antioxidant and methyl donor properties ofbetaine in levodopa/benserazide-mediated hyperhomocysteinemiaand levodopa-induced oxidative stress in rat's kidney wereexamined. METHODS: Sprague-Dawley male rats were dividedinto levodopa (LD), Betaine (Bet.), levodopa plus betaine(LD/Bet.), levodopa plus benserazide (LD/Ben.), levodopa plusbetaine-benserazide (LD/Bet.-Ben.), and control groups. Theexperimental groups received LD (3 × 100 mg/kg), Bet. (1.5%w/w of the total diet), Ben. (3 × 25 mg/kg), and distilled waterwas given to controls for 10 consecutive days, orally by gavage.RESULTS: Plasma total homocysteine (tHcy) concentrationdecreased significantly in Bet.-, LD/Bet.-, and LD/Bet.-Ben.-treated rats compared to LD/Ben. group. Thiobarbituric acidreactive substances concentration (as a lipid peroxidationmarker) in renal tissue reduced statistically in betaine group incomparison with LD and LD/Ben. groups. Renal catalaseactivity increased significantly in LD-treated rats whencompared to controls. Renal superoxide dismutase activitysignificantly decreased in LD-treated group when compared toLD/Ben. group. However, there was not any significantdifference in renal glutathione peroxidase (GPx) activity amongthe groups. CONCLUSIONS: These findings indicate that LD andLD/Ben. have side effects in kidney due to induction ofhyperhomocysteinemia and oxidative stress. In contrast, betaineacts as a promising antioxidant and methyl donor agent versusLD-induced complications.
اظهر المزيد [+] اقل [-]Evaluation of Betaine Neuroprotective Effects on 6-Hydroxydopamine-Induced hemi-Parkinsonism in Male Wistar Rats
2019
Rahmani, Behrouz | Zendehdel, Morteza | Babapour, Vahab | Sadeghinezhad, Javad | Alirezaei, Masoud
BACKGROUND: Parkinson's disease (PD) is one of the prevalent debilitating neurodegenerative disor- ders. Accordingly, researchers are working on methods to modify PD progression. Previously, the neuro- protective effects of betaine, as a methyl donor agent in homocysteine metabolism, have been demonstrated in animal models of chronic cerebral hypoperfusion and memory deficits. OBJECTIVES: It was aimed to investigate the neuroprotective effects of betaine in an animal model of PD. METHODS: In male Wistar rats under two-week course of oral betaine administration (50, 100, and 200 mg/kg per day), the behavioral, biochemical, and histological evaluations were conducted one week follow- ing unilateral nigral 6-OHDA injection. RESUTLS: Betaine administration with dose of 200 mg/kg, one week before and after 6-OHDA lesioning, was associated with a meaningful reduction in the plasma levels of homocysteine (Hcy) in comparison with the control and sham groups (P < 0.05). Our evaluations revealed a remarkable improvement in motor asymmetry induced by apomorphine in the rats under treatment of betaine 200 mg/kg. Moreover, in this group, a significant decrease of malondyaldehyde (MDA) concentrations was detected in the brain tissues, as well as a significantly diminished neuronal cell loss (percent) in substantia nigra pars compacta (P < 0.05). The results of 50 and 100 mg/kg betaine groups were not significant. CONCLUSIONS: Altogether, our findings indicate the antioxidant neuroprotective effects of betaine in this animal model of PD and it is in concordance with betaine properties in decreasing the plasma levels and possible neurotoxic effects of Hcy.
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