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Some studies on the rodenticidal action of indomethacin

E K Omogbai1, R I Ozolua, P E Idaewor

  • 1Department of Pharmacology & Toxicology, University of Benin, Nigeria.

Insights

Indomethacin toxicity in rats is dose-dependent, with an oral LD50 of 12.58 mg/kg. Cholestyramine significantly protected rats from lethal indomethacin doses, reducing mortality by 50%.

Area of Science:

  • Pharmacology
  • Toxicology
  • Gastroenterology

Background:

  • Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID) known for its potential gastrointestinal toxicity.
  • Understanding the dose-response relationship and protective factors is crucial for safe clinical use.

Purpose of the Study:

  • To determine the oral lethal dose 50% (LD50) of indomethacin in rats.
  • To investigate the protective effects of cholestyramine against indomethacin-induced lethality and gastrointestinal lesions.
  • To explore the influence of diazepam and phenobarbital on indomethacin toxicity.

Main Methods:

  • Oral administration of indomethacin to rats to establish LD50 and LD10 values.
  • Administration of cholestyramine, diazepam, and phenobarbital in conjunction with indomethacin.
  • Gross pathological examination of gastrointestinal tissues to assess ulceration and perforation.
  • Comparison of lesion severity in starved, bile duct-ligated, sham-operated, and cholestyramine-treated rats.

Main Results:

  • The oral LD50 of indomethacin was determined to be 12.58 +/- 1.15 mg/kg in rats.
  • Cholestyramine (2 g/kg/day) provided 50% protection against the LD100 of indomethacin.
  • Dose-dependent gastric ulceration and perforation were observed, exacerbated in starved rats and reduced in bile duct-ligated and cholestyramine-treated rats.
  • Diazepam and phenobarbital did not influence indomethacin-induced mortality at the tested doses.

Conclusions:

  • Indomethacin-induced lethality and gastrointestinal damage in rats are dose-dependent.
  • Cholestyramine demonstrates significant protective effects against indomethacin toxicity, likely by binding the drug in the gastrointestinal tract.
  • Further research into cholestyramine as an adjunct therapy for NSAID-induced gastrointestinal injury is warranted.

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