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Comparative Analysis of the Effect of Uridine on Oxidative and Energy Metabolism in the Blood during Administration

N V Khunderyakova1, T V Polyakova2, V P Medvedeva2

  • 1Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Russia. nkhunderyakova@gmail.com.

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Summary

Uridine supplementation reduced key enzyme hyperactivity and oxidative stress in rat models of Parkinson's disease. This neuroprotective effect is linked to the mitochondrial K-ATP channel, suggesting a novel therapeutic target.

Keywords:
Parkinson’s diseaselactate dehydrogenaselymphocytesrotenonesuccinate dehydrogenase

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Area of Science:

  • Neuroscience and Neurodegenerative Diseases
  • Biochemistry and Metabolism
  • Pharmacology

Background:

  • Parkinson's disease models (rotenone and 6-OHDA) exhibit elevated succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH) activity in lymphocytes.
  • These models also show increased lipid peroxidation (LPO) products in blood serum, indicating heightened oxidative stress.
  • Mitochondrial dysfunction is a key feature in Parkinson's pathogenesis.

Purpose of the Study:

  • To investigate the therapeutic potential of uridine on oxidative metabolism and key enzyme activities in Parkinson's disease models.
  • To explore the role of the mitochondrial K-ATP channel (mitoKATP) in mediating uridine's effects.
  • To assess uridine's impact on lymphocyte enzyme activity and serum oxidative stress markers.

Main Methods:

  • Utilized rotenone and 6-OHDA rat models to simulate Parkinson's disease.
  • Administered uridine (30 mg/kg) for 28 days and assessed SDH and LDH activities in lymphocytes.
  • Measured serum lipid peroxide (LPO) levels and evaluated the effect of the mitoKATP inhibitor 5-hydroxydecanoate.

Main Results:

  • Uridine treatment significantly mitigated the hyperactivation of SDH and LDH in lymphocytes of Parkinson's disease models.
  • Uridine administration led to a reduction in serum LPO products, alleviating oxidative stress.
  • The protective effects of uridine were abolished by the specific mitoKATP inhibitor, 5-hydroxydecanoate.

Conclusions:

  • Uridine demonstrates neuroprotective effects in Parkinson's disease models by normalizing lymphocyte enzyme activity and reducing oxidative stress.
  • The mitochondrial K-ATP channel (mitoKATP) plays a crucial role in mediating the beneficial actions of uridine.
  • Targeting mitoKATP with uridine presents a potential therapeutic strategy for Parkinson's disease.