Protective role of zeaxanthin on acrylamide-induced neurotoxicity in Wistar rats
Objective: The Maillard reaction generates acrylamide (ACR), a toxic compound commonly found in laboratory and industrial settings. ACR exposure, both short-term and long-term, can damage various organs, notably the central nervous system, through oxidative stress, inflammation, and apoptosis. This...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Mashhad University of Medical Sciences
2025-03-01
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| Series: | Avicenna Journal of Phytomedicine |
| Subjects: | |
| Online Access: | https://ajp.mums.ac.ir/article_24950_9e01603b7cf9454e6babb180ee338066.pdf |
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| Summary: | Objective: The Maillard reaction generates acrylamide (ACR), a toxic compound commonly found in laboratory and industrial settings. ACR exposure, both short-term and long-term, can damage various organs, notably the central nervous system, through oxidative stress, inflammation, and apoptosis. This study explores the potential neuroprotective effects of zeaxanthin (ZEA), known for its antioxidant, anti-inflammatory, and anti-apoptotic properties, against ACR-induced toxicity in the rat cerebral cortex.Materials and Methods: Rats were subjected to ACR exposure (50 mg/kg, intraperitoneal injection) for 11 days and subsequently, treated with ZEA (20-80 mg/kg, intragastric gavage) for either 11 or 20 days to assess both preventive and therapeutic effects. Locomotor behavior was evaluated using a gait score test, while biochemical analyses measured malondialdehyde (MDA) and glutathione (GSH) levels, inflammatory markers interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α), and apoptotic markers (cleaved caspase-3) in the cerebral cortex.Results: ACR exposure impaired locomotion in the animals, but ZEA treatment significantly improved gait scores when administered preventatively (from days 6-11) or therapeutically (from days 6-20). ACR also led to increased MDA levels and depleted GSH content in brain tissue, and it elevated IL-1β, TNF-α, and cleaved caspase-3 in the cerebral cortex. However, ZEA supplementation, along with vitamin E, effectively reversed these alterations compared to the ACR-exposed group.Conclusion: In conclusion, ZEA demonstrates both preventive and therapeutic effects against ACR-induced neurotoxicity. These findings suggest that ZEA could serve as an effective preventive agent by countering ACR-induced damage through its antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. |
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| ISSN: | 2228-7930 2228-7949 |