Experimental overview showing how Selenomethionine (SeMet) protects N27 dopaminergic cells from 6-hydroxydopamine (6-OHDA)–induced oxidative stress in a dose-dependent manner. Credit: I. Bano / Charles University & NUDZ

Dopamine is often called the brain’s “motivation molecule,” but for me, it represents something deeper, a window into how fragile our neurons can be. The cells that produce dopamine, known as dopaminergic neurons, are among the first to die in Parkinson’s disease, leading to the motor symptoms that gradually rob patients of movement and independence.

To understand what makes these neurons so vulnerable, I used an in-vitro model where I exposed N27 dopaminergic cells to 6-hydroxydopamine (6-OHDA), a toxin that triggers oxidative stress, like what occurs in the Parkinsonian brain. Then, I introduced Selenomethionine (SeMet), an organic form of selenium, to test whether this compound could counteract the damage and help the neurons survive.

Selenium has long intrigued scientists for its paradoxical nature. It is a trace element essential for antioxidant defense, yet in excess it can become toxic. I wanted to see whether a specific range of SeMet concentrations could offer meaningful protection without tipping that balance. My study, carried out at Charles University and the National Institute of Mental Health (NUDZ) in the Czech Republic, set out to define that “safe and effective window.” It is published in the journal In vitro models.

When dopaminergic cells were exposed to 6-OHDA alone, I saw a rapid collapse of antioxidant defenses. Levels of glutathione (GSH) and ascorbic acid (vitamin C) fell sharply, total protein content dropped, and under the microscope, the cells appeared shrunken and detached. However, when I pre-treated them with SeMet, the outcome changed dramatically. The neurons retained their shape and adhesion, and their antioxidant systems recovered in a clear dose-dependent manner.

Quantitative analysis revealed that SeMet concentrations between 10 and 30 µM provided the most consistent protection. Beyond that range, the effect diminished, confirming selenium’s well-known biphasic behavior. Using Coomassie staining, I could visualize how SeMet helped preserve the cytoskeleton the internal scaffolding that maintains a neuron’s structure.

The 6-OHDA-treated cells showed fragmented outlines and weak attachment, while those pre-treated with SeMet looked healthy and intact. For me, these images were more than data points; they were evidence that even highly sensitive neurons can recover stability when given the right molecular support.

This finding defines a potential therapeutic window for selenium-based neuroprotection. If similar results can be reproduced in living systems, SeMet might offer a way to strengthen dopaminergic neurons before irreversible loss occurs. Since Parkinson’s disease is usually diagnosed only after about 60% of these neurons have already died, early protection could change the timeline of intervention from managing decline to preventing it.

My broader research also explores focused ultrasound stimulation (FUS), a noninvasive technique that uses gentle acoustic energy to influence neuronal activity. One exciting prospect is combining FUS with compounds like SeMet to help guide protective molecules across the blood–brain barrier precisely where they are needed.

I believe the future of neuroprotection lies in such hybrid approaches, where biochemistry and physics work hand in hand to preserve brain function. Every time I look through the microscope and see SeMet-treated neurons still attached, still glowing with life, I am reminded that survival in biology often comes down to balance. For dopaminergic neurons and perhaps for the future of Parkinson’s, that balance might be found in something as small and precise as the right dose of selenium.

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More information: Iqra Bano et al, In vitro study of selenomethionine’s concentration-dependent effects in a 6-OHDA model of Parkinson’s disease, In vitro models (2025). DOI: 10.1007/s44164-025-00095-6

Dr. Iqra Bano is a doctoral researcher at the Department of Animal Physiology, Faculty of Science, Charles University, and an R1 researcher at the National Institute of Mental Health (NUDZ) in the Czech Republic. Originally from Sindh, Pakistan, she is currently based in Europe, where her research focuses on neurodegenerative diseases, particularly Parkinson’s disease. Dr. Bano is an active contributor to the European Union Joint Program Neurodegenerative Disease Research (JPND) project Restoring Motor Functions in Parkinson’s Disease with Noninvasive Hybrid Transcranial Neuromodulation (REMOPD). Her ongoing research, in collaboration with Dr. Grygoriy Tsenov and Dr. Jaison Jeevanandam at NUDZ, integrates neurochemistry, nanotechnology, and cellular neurophysiology by evaluating the effects of selenium-derived nanoparticles, organic selenium compounds, and FUS-mediated calcium signaling as potential neuroprotective strategies.

Citation: The right dose for the brain: Selenomethionine’s role in protecting dopaminergic neurons (2025, November 3) retrieved 3 November 2025 from https://medicalxpress.com/news/2025-11-dose-brain-selenomethionine-role-dopaminergic.html

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