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Induction of emesis in Suncus murinus by pyrogallol, a generator of free radicals
1Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Abstract:
1. We investigated whether or not pyrogallol, a generator of free radicals, is emetogenic in Suncus murinus, the house musk shrew. Pyrogallol (i.p.) caused dose-dependent emesis in suncus with an ED50 value of 77.3 mg kg-1. At a dose of 128 mg kg-1, all suncus vomited with mean latency of 18.8 +/- 5.2 min and the number of vomiting episodes was 8.6 +/- 2.9. 2. The prophylactic effects of N-(2-mercaptopropionyl)-glycine (MPG), an antioxidant, and tropisetron, a 5-hydroxytryptamine3 (5-HT3) receptor antagonist, were studied. Pyrogallol (128 mg kg-1, i.p.)-induced emesis was prevented by treatment with MPG (i.p.) or tropisetron (s.c.) with ID50 values of 149 mg kg-1 and 117 micrograms kg-1, respectively. 3. Pyrogallol-induced emesis was completely prevented by surgical abdominal vagotomy. 4. The present results indicate that pyrogallol-induced emesis is characteristically very similar to that caused by cisplatin and support the idea that generation of free radicals causes the release of peripheral 5-HT, which stimulates vagal afferent sensory nerves to cause emesis.
Insights
Pyrogallol causes dose-dependent vomiting in shrews by generating free radicals. This effect, mediated by the vagal nerve and serotonin release, can be blocked by antioxidants and specific receptor antagonists.
Area of Science:
- Pharmacology
- Gastroenterology
- Neuroscience
Background:
- Free radicals are implicated in various physiological processes.
- The emetogenic potential of pyrogallol, a free radical generator, has not been fully elucidated.
- Understanding emesis mechanisms is crucial for developing anti-emetic therapies.
Purpose of the Study:
- To investigate the emetogenic effects of pyrogallol in Suncus murinus.
- To explore the prophylactic potential of an antioxidant (MPG) and a 5-HT3 receptor antagonist (tropisetron) against pyrogallol-induced emesis.
- To determine the role of the vagal nerve in pyrogallol-induced emesis.
Main Methods:
- Administration of pyrogallol (i.p.) to Suncus murinus to assess emesis.
- Prophylactic treatment with N-(2-mercaptopropionyl)-glycine (MPG) and tropisetron.
- Surgical abdominal vagotomy in Suncus murinus.
- Dose-response analysis to determine ED50 and ID50 values.
Main Results:
- Pyrogallol induced dose-dependent emesis in Suncus murinus (ED50 = 77.3 mg kg-1).
- MPG (ID50 = 149 mg kg-1) and tropisetron (ID50 = 117 μg kg-1) significantly prevented pyrogallol-induced emesis.
- Abdominal vagotomy completely abolished pyrogallol-induced emesis.
Conclusions:
- Pyrogallol-induced emesis in Suncus murinus shares characteristics with cisplatin-induced emesis.
- Free radical generation by pyrogallol likely triggers peripheral serotonin release, stimulating vagal afferent nerves to induce vomiting.
- These findings support the role of free radicals and serotonin in emesis and suggest potential therapeutic targets.