(PO19-04-22) Neuroprotective Function of Fucoxanthin in Oxidative Stress-Mediated Mitochondrial Dysfunction

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Presenting Author(s)

KF

Khondoker Adeba Ferdous, M.S
– Doctoral Student, University of Alabama, Tuscaloosa, Alabama, United States

Co-Author(s)

GB

Garret Burnett, n/a
– University of Alabama, Tusclaoosa, Alabama, United States
Madison L. Scott
– Student, University of Alabama, Madison, Alabama, United States
EA

Emma Amjad, n/a
– University of Alabama, Tuscaloosa, Alabama, United States
SB

Sydni Bannerman, n/a
– University of Alabama, Tusclaoosa, Alabama, United States
HP

Han-A Park, PhD
– Assistant Professor, University of Alabama, Tusclaoosa, Alabama, United States

Disclosure(s):

Khondoker Adeba Ferdous, M.S: No relevant financial relationship(s) with ineligible companies to disclose.

Han-A Park, PhD: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: Oxidative stress plays an important role in neuronal loss associated with mitochondrial dysfunction. Excess reactive oxygen species (ROS) production damages mitochondria, impairing neuronal energy metabolism. The damaged mitochondria promote aberrant ROS production leading to neuronal death. Fucoxanthin, a carotenoid with antioxidant properties primarily found in brown seaweeds, has been shown to protect mitochondria in various disease models. However, limited studies have demonstrated the mechanisms of fucoxanthin-mediated neuroprotection. In this study, we hypothesize that fucoxanthin regulates DJ-1, an oxidative stress sensing protein, and protects neurons against ROS-mediated mitochondrial dysfunction.

Methods: Rat primary hippocampal neurons were treated with fucoxanthin, hydrogen peroxide, or a combination of both. After 6h of incubation, mitochondrial superoxide and the mitochondrial membrane potential were measured using mitoSOX and TMRM, respectively. Middle-aged male Sprague Dawley rats were supplemented with or without fucoxanthin (1mg/kg, 5d/w for 4wk). After supplementation was completed, brain tissues were harvested, and DJ-1 protein levels were quantified using immunoblotting.

Results: Treatment with fucoxanthin decreased mitochondrial superoxide accumulation and prevented loss of mitochondrial membrane potential against ROS challenge in rat primary hippocampal neurons. Oral supplementation of fucoxanthin increased DJ-1 protein levels in the hippocampal tissues isolated from middle-aged rats.

Conclusions: We found that fucoxanthin treatment upregulates DJ-1 expression in the hippocampus in vivo and protects mitochondria during ROS challenges in primary hippocampal neurons in vitro. Our data suggest fucoxanthin has neuroprotective potential against ROS-associated mitochondrial dysfunction.

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