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Mitochondrial Ultrastructure, Fission Proteins, Activity, and Motor Dysfunctions in the Innovative Parkinson's

Cesar Alfonso Garcia-Caballero1,2, Jose Luis Ordoñez-Librado2, Avril De Alba-Ríos2

  • 1Unidad de Posgrado, Edificio "D", Primer Piso, Cto. de los Posgrados S/N, C.U., Postgraduate Unit, Building "D", First Floor, Postgraduate Circuit S/N, C.U., Coyoacan, Mexico City 04510, Mexico.

Toxics
|March 27, 2026
PubMed

Insights

Manganese inhalation in mice causes Parkinson's-like motor deficits and mitochondrial dysfunction. This model effectively mimics key Parkinson's disease (PD) pathology, aiding research into new treatments.

Area of Science:

  • Neuroscience
  • Toxicology
  • Mitochondrial Biology

Background:

  • Parkinson's disease (PD) pathogenesis is not fully understood, necessitating robust experimental models.
  • Mitochondrial dysfunction is a critical mechanism implicated in PD.
  • Previous research established a manganese inhalation model for PD, but its impact on mitochondria was unexplored.

Purpose of the Study:

  • To investigate the effects of manganese inhalation on mitochondrial function in a mouse model of PD.
  • To assess mitochondrial ultrastructure, protein expression (fission/fusion), and electron transport chain complex activity.
  • To correlate these molecular changes with motor performance deficits.

Main Methods:

  • Male CD1 mice were exposed to a manganese mixture (MnCl2 and Mn(OAc)3) via inhalation twice weekly for five months.
  • Control mice received deionized water.
  • Evaluated mitochondrial morphology, Drp1/Fis1 protein levels, electron transport chain complex I and IV activity, and fine motor performance.

Main Results:

  • Manganese inhalation induced significant fine motor deficits in mice.
  • Mitochondria showed increased numbers, reduced area, altered circularity, and disorganized cristae.
  • Elevated Drp1 and Fis1 levels were observed, along with decreased activity of electron transport chain complexes I and IV, particularly in the substantia nigra pars compacta (SNc).

Conclusions:

  • The manganese inhalation model replicates key mitochondrial and motor deficits observed in Parkinson's disease.
  • This progressive, bilateral model is suitable for evaluating mitochondria-targeted therapeutic strategies for PD.
  • The findings underscore the role of mitochondrial dysfunction in manganese-induced neurotoxicity relevant to PD.
Keywords:
Drp1Fis1Parkinson’s diseaseanimal modelmanganesemitochondriamitochondrial activityultrastructure

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