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Cimetidine: antioxidant and metal-binding properties.
Zaynab Lambat1, Janice L Limson, Santy Daya
1Faculty of Pharmacy, Rhodes University, Box 94 Grahamstown, 6140, South Africa.
The Journal of Pharmacy and Pharmacology
|January 25, 2003
Summary
Cimetidine, a potent H(2) receptor antagonist, demonstrates antioxidant properties by reducing free radical generation. It protects against iron-induced damage in brain homogenates, suggesting neuroprotective effects.
Area of Science:
- Pharmacology
- Neuroscience
- Biochemistry
Background:
- Cimetidine is a widely used H(2) receptor antagonist for treating peptic ulcers.
- Excessive free radical generation, particularly in the brain, contributes to oxidative stress and neuronal damage.
- Iron is a key catalyst in free radical production via reactions like the Fenton reaction.
Purpose of the Study:
- To investigate the antioxidant capacity of cimetidine.
- To determine if cimetidine can mitigate iron-induced free radical generation and lipid peroxidation in brain tissue.
- To explore the potential neuroprotective mechanisms of cimetidine.
Main Methods:
- Nitroblue-tetrazolium assay to assess superoxide anion generation.
- Lipid peroxidation assays using rat brain homogenates to measure oxidative damage.
- Electrochemical, UV/Vis spectroscopy, and HPLC to analyze metal-ligand interactions.
Main Results:
- Cimetidine significantly reduced superoxide anion generation in the nitroblue-tetrazolium assay.
- Cimetidine inhibited the iron-induced increase in lipid peroxidation in rat brain homogenates.
- Evidence of metal-ligand interactions between cimetidine and transition metals (iron, copper) was observed.
Conclusions:
- Cimetidine exhibits significant antioxidant activity.
- Cimetidine's ability to bind to transition metals like iron and copper prevents their involvement in free radical production.
- These findings suggest a neuroprotective role for cimetidine through its antioxidant and metal-chelating properties.