Guanidinoacetate alters antioxidant defenses and butyrylcholinesterase activity in the blood of rats
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 o...
| Authors: | , , , , , , , |
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| Format: | article |
| Status: | Published version |
| Publication Date: | 2015 |
| Country: | Brasil |
| Institution: | Universidade Federal do Rio Grande do Sul (UFRGS) |
| Repository: | Clinical and Biomedical Research |
| Language: | English |
| OAI Identifier: | oai:seer.ufrgs.br:article/52197 |
| Online Access: | https://seer.ufrgs.br/index.php/hcpa/article/view/52197 |
| Access Level: | Open access |
| Keyword: | Butyrylcholinesterase glutathione guanidinoacetate L-NAME TBARS trolox |
| Summary: | 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. |
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