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Purpose <p>Parkinson’s disease (PD) is characterized by oxidative stress-induced degeneration of dopaminergic neurons. This study evaluated the concentration-related neuroprotective effects of Selenomethionine (SeMet) against 6-hydroxydopamine (6-OHDA)- induced toxicity using an in vitro model of N27 dopaminergic cells. In vitro models provide an essential platform for identifying therapeutic candidates and elucidating cellular mechanisms before validation in animal models.</p> Methods <p>N27 cells were pretreated with SeMet (2, 10, or 30&#xa0;µM) followed by 30&#xa0;µM 6-OHDA exposure. Intracellular glutathione (GSH) and ascorbic acid levels were quantified. Cell viability was assessed using the Trypan blue exclusion assay. Protein content and morphology were evaluated via Coomassie staining and ImageJ-based morphometric analysis.</p> Results <p>6-OHDA significantly reduced GSH (0.0044 ± 0.0005&#xa0;µM) and ascorbic acid (3.28 ± 0.55&#xa0;µM) compared to control. Pretreatment with 30&#xa0;µM SeMet significantly restored GSH (0.0330 ± 0.0076&#xa0;µM; <i>p</i> &lt; 0.01*) and ascorbic acid (4.59 ± 0.93&#xa0;µM; <i>p</i> &lt; 0.05*). Cell viability declined to 44.0 ± 2.34% with 6-OHDA but improved significantly with 30&#xa0;µM SeMet co-treatment (81.3 ± 9.82%; <i>p</i> &lt; 0.001***), although 10&#xa0;µM was found to be the most effective overall, consistent with the biphasic concentration response of selenium compounds. Protein content dropped to 8.05 ± 4.50 AU with 6-OHDA and recovered with SeMet (70.21 ± 24.59 AU). Integrated density analysis and morphology confirmed cellular protection.</p> Conclusion <p>These in vitro findings demonstrate that SeMet exerts concentration-dependent neuroprotective effects against 6-OHDA-induced oxidative stress in N27 cells. The highest concentration of SeMet (30&#xa0;µM) offered optimal protection, supporting SeMet’s therapeutic potential for early-stage PD intervention strategies.</p>

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In vitro study of selenomethionine’s concentration-dependent effects in a 6-OHDA model of Parkinson’s disease

  • 期刊论文

  • 发表日期：

    2025年10月28日

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  • Iqra Bano,
  • Jaison Jeevanandam,
  • Grygoriy Tsenov

摘要

Purpose

Parkinson’s disease (PD) is characterized by oxidative stress-induced degeneration of dopaminergic neurons. This study evaluated the concentration-related neuroprotective effects of Selenomethionine (SeMet) against 6-hydroxydopamine (6-OHDA)- induced toxicity using an in vitro model of N27 dopaminergic cells. In vitro models provide an essential platform for identifying therapeutic candidates and elucidating cellular mechanisms before validation in animal models.

Methods

N27 cells were pretreated with SeMet (2, 10, or 30 µM) followed by 30 µM 6-OHDA exposure. Intracellular glutathione (GSH) and ascorbic acid levels were quantified. Cell viability was assessed using the Trypan blue exclusion assay. Protein content and morphology were evaluated via Coomassie staining and ImageJ-based morphometric analysis.

Results

6-OHDA significantly reduced GSH (0.0044 ± 0.0005 µM) and ascorbic acid (3.28 ± 0.55 µM) compared to control. Pretreatment with 30 µM SeMet significantly restored GSH (0.0330 ± 0.0076 µM; p < 0.01*) and ascorbic acid (4.59 ± 0.93 µM; p < 0.05*). Cell viability declined to 44.0 ± 2.34% with 6-OHDA but improved significantly with 30 µM SeMet co-treatment (81.3 ± 9.82%; p < 0.001***), although 10 µM was found to be the most effective overall, consistent with the biphasic concentration response of selenium compounds. Protein content dropped to 8.05 ± 4.50 AU with 6-OHDA and recovered with SeMet (70.21 ± 24.59 AU). Integrated density analysis and morphology confirmed cellular protection.

Conclusion

These in vitro findings demonstrate that SeMet exerts concentration-dependent neuroprotective effects against 6-OHDA-induced oxidative stress in N27 cells. The highest concentration of SeMet (30 µM) offered optimal protection, supporting SeMet’s therapeutic potential for early-stage PD intervention strategies.