Developing a non-invasive animal model for oxidative stress induced brain damage : towards evaluating beneficial therapeutics for the brain.
The brain is particularly sensitive to oxidative stress damage due to high oxygen consumption, high contents of peroxidizable polyunsaturated fatty acid and low levels of antioxidants. Resultant overt oxidative stress is a main causative agent of neurodegenerative diseases. Currently, no animal mode...
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Format: | Final Year Project |
Language: | English |
Published: |
2013
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Online Access: | http://hdl.handle.net/10356/53281 |
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Institution: | Nanyang Technological University |
Language: | English |
Summary: | The brain is particularly sensitive to oxidative stress damage due to high oxygen consumption, high contents of peroxidizable polyunsaturated fatty acid and low levels of antioxidants. Resultant overt oxidative stress is a main causative agent of neurodegenerative diseases. Currently, no animal model exists that allows non-invasive induction of oxidative stress and continuous monitoring of elicited neural damage. Zebrafish larvae expressing the genetically encoded photosensitizer, KillerRed, in various brain domains creates such an opportunity. Non-invasive induction of oxidative stress triggered by green light illumination increased ROS production in the brain of illuminated SqKR21 transgenic line. This was confirmed with the oxidation-sensitive BODIPY® 581/591 C11 sensor. Induced ROS further attacked KR’s chromophore, which resulted in 1.8 fold decrease in KR fluorescent intensity. Concomitantly, ROS induced brain damage reduced neural growth in the developing larvae. These three criteria were used to assess antioxidants efficacy. Curcumin is the only tested antioxidant that improved KR fluorescent intensity in a statistically significant manner. However improvement in neural growth was minimal. The research detailed the setting up of the non-invasive brain oxidative stress model and established criteria that must be scored to identify beneficial antioxidants that improved the physiology of oxidative stress derived neurological disorders. |
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