Guanidinoacetate alters antioxidant defenses and butyrylcholinesterase activity in the blood of rats
| Autor: | Guilherme André Eger, Vinícius Vialle Ferreira, Camila Ribeiro Batista, Daniela Delwing de Lima, Angela Terezinha de Souza Wyse, Júlia Niehues da Cruz, Débora Delwing Dal Magro, José Geraldo Pereira da Cruz |
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| Jazyk: | English<br />Portuguese |
| Rok vydání: | 2015 |
| Předmět: | |
| Zdroj: | Clinical and Biomedical Research, Vol 35, Iss 1 (2015) |
| Druh dokumentu: | article |
| ISSN: | 0101-5575 2357-9730 |
| Popis: | Deficiency of guanidinoacetate methyltransferase, the first described creatine biosynthesis defect, leads to depletion of creatine and phosphocreatine, and accumulation of guanidinoacetate (GAA) in brain and body fluids. The present study aimed to investigate the influence of GAA on the activities of antioxidant enzymes, as well as on thiobarbituric acid-reactive substances (TBARS) and butyrylcholinesterase (BuChE) activity in the blood of rats. Results showed that GAA enhanced the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in the erythrocytes and BuChE activity. In addition, GAA enhanced TBARS levels in the plasma. Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), GSH (glutathione) and L-NAME (NG-nitro-L-arginine methyl ester) addition prevented the majority of alterations in oxidative stress parameters and the increase of BuChE activity that were caused by GAA. Data suggest that GAA alters antioxidant defenses and induces lipid peroxidation in the blood, as well altering BuChE activity. However, in the presence of trolox, GSH and L-NAME some of these alterations in oxidative stress and BuChE activity were prevented. Our findings lend support to a potential therapeutic strategy for this condition, which may include the use of appropriate antioxidants for ameliorating the damage caused by GAA. |
| Databáze: | Directory of Open Access Journals |
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