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Development of an animal model for chronic mild hyperhomocysteinemia and its response to oxidative damage
Emilene B S Scherer1, Aline Andrea da Cunha, Janaína Kolling
1Laboratório de Neuroproteção e Doenças Metabólicas, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Abstract:
The purpose of this study was to develop a chronic chemically induced model of mild hyperhomocysteinemia in adult rats. We produced levels of Hcy in the blood (30μM), comparable to those considered a risk factor for the development of neurological and cardiovascular diseases, by injecting homocysteine subcutaneously (0.03μmol/g of body weight) twice a day, from the 30th to the 60th postpartum day. Controls received saline in the same volumes. Using this model, we evaluated the effect of chronic administration of homocysteine on redox status in the blood and cerebral cortex of adult rats. Reactive oxygen species and thiobarbituric acid reactive substances were significantly increased in the plasma and cerebral cortex, while nitrite levels were reduced in the cerebral cortex, but not in the plasma, of rats subjected to chronic mild hyperhomocysteinemia. Homocysteine was also seen to disrupt enzymatic and non-enzymatic antioxidant defenses in the blood and cerebral cortex of rats. Since experimental animal models are useful for understanding the pathophysiology of human diseases, the present model of mild hyperhomocysteinemia may be useful for the investigation of additional mechanisms involved in tissue alterations caused by homocysteine.
Insights
This study developed a rat model for mild hyperhomocysteinemia, a risk factor for neurological and cardiovascular diseases. The model revealed homocysteine disrupts antioxidant defenses and redox balance in blood and brain tissues.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Toxicology
Background:
- Mild hyperhomocysteinemia is a risk factor for neurological and cardiovascular diseases.
- Existing models may not fully replicate chronic, mild elevations of homocysteine.
- Understanding the impact of homocysteine on redox status is crucial for disease research.
Purpose of the Study:
- To develop and validate a chronic chemically induced model of mild hyperhomocysteinemia in adult rats.
- To investigate the effects of chronic mild hyperhomocysteinemia on redox status and antioxidant defenses in blood and the cerebral cortex.
- To provide a valuable tool for studying homocysteine-induced pathophysiology.
Main Methods:
- Adult rats were injected subcutaneously with homocysteine (0.03 μmol/g body weight) twice daily from day 30 to 60 postpartum.
- Control groups received saline injections.
- Redox status (reactive oxygen species, thiobarbituric acid reactive substances, nitrite) and antioxidant defenses were assessed in plasma and cerebral cortex.
Main Results:
- The model successfully induced mild hyperhomocysteinemia (30 μM Hcy) in rats.
- Chronic homocysteine administration significantly increased reactive oxygen species and thiobarbituric acid reactive substances in plasma and cerebral cortex.
- Nitrite levels were reduced in the cerebral cortex, and both enzymatic and non-enzymatic antioxidant defenses were disrupted.
Conclusions:
- The developed rat model effectively mimics chronic mild hyperhomocysteinemia.
- Homocysteine significantly alters redox balance and impairs antioxidant defenses in the blood and brain.
- This model serves as a valuable resource for further research into homocysteine-related tissue damage and disease mechanisms.
