Fucoxanthin and its metabolite fucoxanthinol alleviate paraquat-induced oxidative damage and neurotoxicity in differentiated human neuroblastoma cells

Funding Sponsor

Northern Border University

Fourth Author's Department

Institute of Global Health & Human Ecology

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https://doi.org/10.1080/16583655.2025.2512661

All Authors

Ekramy M. Elmorsy Ayat B. Al-Ghafari Huda A. Al Doghaither Mohamed M. Salama Hanaa M. Elzahed Raed AlRuwaili

Document Type

Research Article

Publication Title

Journal of Taibah University for Science

Publication Date

1-1-2025

doi

10.1080/16583655.2025.2512661

Abstract

Paraquat (PQ), a widely used herbicide, is linked to increased Parkinson's disease (PD) risk. This study explored the neuroprotective effects of fucoxanthin (FX) and its metabolite fucoxanthinol (FXL) in a differentiated dopaminergic neuron model. PQ exposure (10 µM) for 72 hours reduced cell viability (EC50 = 10 µM), impaired noradrenaline uptake, increased oxidative stress, disrupted mitochondrial function and triggered apoptosis. Specifically, PQ reduced ATP levels, mitochondrial membrane potential and enzyme activities, while elevating lactate, reactive oxygen species and caspase expression. It also suppressed antioxidant enzymes and the gene expression of Nrf2 and Ho-1. Co-treatment with FX or FXL (2.5–5 µM) significantly countered PQ's harmful effects, improving cell viability, restoring neurotransmitter function, enhancing mitochondrial activity, reducing oxidative damage and inhibiting apoptosis. FXL showed stronger protective effects than FX. These findings highlight the therapeutic potential of FX and FXL in mitigating PQ-induced neurotoxicity and suggest their promise in PD prevention and treatment.

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