(P27-012-23) Does Fucoxanthin Help in the Fight Against Aging-Associated Oxidative Stress in the Brain?

Objectives: Oxidative stress is a major cause of cellular dysfunction during aging. Notably, cells in the brain are vulnerable to lipid peroxidation, because the brain is rich in phospholipids and sphingolipids and is highly dependent on oxidative phosphorylation to carry out its metabolic demands. Fucoxanthin, a type of carotenoid, is a hydrophobic antioxidant found in brown seaweed. Previously, fucoxanthin has been shown to be protective against various brain-associated disorders. However, the role of fucoxanthin in the brain during aging has not been fully explored. In this study, we hypothesized that treatment with fucoxanthin protects the brain from aging-associated oxidative stress. In particular, we test whether fucoxanthin regulates the abundance of DJ1, an oxidative stress sensor protein that plays a critical role in neuronal energy metabolism.

Methods: Middle-aged male Sprague Dawley rats were orally gavaged with fucoxanthin (1 mg/kg, 5 d/w) or control oil for 4 weeks. After the completion of supplementation, tissues from the control and fucoxanthin-supplemented animals were harvested. Levels of lipid peroxidation in the brain were evaluated using TBARS, and the protein levels of DJ1 were quantified using immunoblotting. We further cultured the rat primary hippocampal neurons in vitro. Neurons were grown in neurobasal media with or without fucoxanthin for 6 weeks. Cell viability was assessed by PI staining. Mitochondrial membrane potential and mitochondrial superoxide levels were assayed using TMRM and mitoSOX, respectively.

Results: Oral supplementation of fucoxanthin decreased lipid peroxidation and increased the DJ1 protein in the brain. Treatment with fucoxanthin decreased aging-associated cell death, the loss of mitochondrial membrane potential, and the accumulation of superoxide in primary hippocampal neurons.

Conclusions: Our findings suggest that fucoxanthin may delay aging-mediated neuronal damage or potentially protect the brain against neurotoxic insults associated with oxidative stress. Future investigations on kinetics and bioavailability of fucoxanthin in the brain may be critical in translational research.

Funding Sources: RGC Program (University of Alabama); Crenshaw Research Fund (University of Alabama)