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 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 (۵۰ mg/kg, intraperitoneal injection) for ۱۱ days and subsequently, treated with ZEA (۲۰-۸۰ mg/kg, intragastric gavage) for either ۱۱ or ۲۰ 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-۱ beta (IL-۱β), and tumor necrosis factor-alpha (TNF-α), and apoptotic markers (cleaved caspase-۳) in the cerebral cortex.Results: ACR exposure impaired locomotion in the animals, but ZEA treatment significantly improved gait scores when administered preventatively (from days ۶-۱۱) or therapeutically (from days ۶-۲۰). ACR also led to increased MDA levels and depleted GSH content in brain tissue, and it elevated IL-۱β, TNF-α, and cleaved caspase-۳ 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.

کلیدواژه ها:

Acrylamide ، Zeaxanthin ، Antioxidant ، Anti-inflammatory ، Apoptosis ، Neuroprotective agents