Protective effect of adenosine in rat model of Parkinson's disease: Neurobehavioral and neurochemical evidences

Khan Shoeb Zafar, Almas Siddiqui, Iqbal Sayeed, Muzamil Ahmad, Sofiyan Saleem, Fakhrul Islam

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Normal cellular metabolism produces oxidants which are neutralized within the cell by antioxidant enzymes and other antioxidants. An imbalance between oxidant and antioxidant has been postulated to lead the degeneration of dopaminergic neurons in Parkinson's disease. In this study, we examined whether adenosine, an antioxidant, can prevent or slowdown neuronal injury in 6-hydroxydopamine (6-OHDA) model of Parkinsonism. Rats were treated with adenosine (500, 250, 125 mg/kg b.wt.) once before surgery and five times after surgery (1 h interval). 2 μl 6-OHDA (12.5 μg in 0.2% ascorbic acid in normal saline) was infused in the right striatum. Two weeks after 6-OHDA infused rats were tested for neurobehavioral activity and sacrificed after 3 weeks of 6-OHDA infusion, for the estimation of glutathione peroxidase, glutathione-S-transferase, glutathione reductase, glutathione content, lipid peroxidation and dopamine and its metabolites. Adenosine was found to be successful in up-regulating the antioxidant status, lowering the dopamine loss and functional recovery returned close to the baseline dose. This study revealed that adenosine, which is an essential part of our body, might be helpful in slowing down the progression of neurodegeneration in Parkinsonism.

Original languageEnglish (US)
Pages (from-to)143-151
Number of pages9
JournalJournal of Chemical Neuroanatomy
Issue number2
StatePublished - Oct 2003
Externally publishedYes


  • 6-Hydroxydopamine
  • Adenosine
  • Dopaminergic neurodegeneration
  • Glutathione
  • Neuroprotection
  • Oxidative stress
  • Parkinson's disease

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


Dive into the research topics of 'Protective effect of adenosine in rat model of Parkinson's disease: Neurobehavioral and neurochemical evidences'. Together they form a unique fingerprint.

Cite this