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Carboxylesterases, a key factor in evaluating potential genotoxicity of Trinem antibiotics

J Oliver1, A Naidoo, L Vandin

  • 1Genetic Toxicology Department, Pre-Clinical Safety Sciences, Medicine Safety Evaluation Division, Glaxo Wellcome Research and Development, Park Road, Ware, Herts SG12 0DP, UK. jo3639@glaxowellcome.co.uk

Mutagenesis
|January 21, 2000
PubMed

Insights

Sanfetrinem cilexetil, a Trinem antibiotic, did not show genotoxicity in vivo. The drug is unlikely to pose a genotoxic hazard to humans during therapeutic use due to its rapid hydrolysis.

Area of Science:

  • Pharmacology
  • Toxicology
  • Genetics

Background:

  • Sanfetrinem cilexetil is a Trinem antibiotic hexetil ester.
  • Assessing the genotoxic potential of pharmaceuticals is crucial for drug safety.

Purpose of the Study:

  • To evaluate the in vivo and in vitro genotoxicity of Sanfetrinem cilexetil.
  • To investigate the role of carboxylesterase activity in the genotoxic profile of Sanfetrinem cilexetil.

Main Methods:

  • In vivo micronucleus test in rat bone marrow.
  • In vivo DNA repair synthesis assay in rat hepatocytes.
  • In vitro chromosomal aberration and mutation assays in mammalian cells with and without carboxylesterase activity.
  • In vitro assays with rat liver and intestinal preparations.

Main Results:

  • Sanfetrinem cilexetil did not induce genotoxicity in vivo in rats.
  • In vitro, chromosome damage and mutations were observed in cells lacking carboxylesterase activity.
  • Genotoxicity was abolished in the presence of carboxylesterase activity (CHL cells) or esterase preparations from rat liver and intestinal cells.

Conclusions:

  • The lack of in vivo genotoxicity is attributed to rapid hydrolysis by intestinal carboxylesterases.
  • Sanfetrinem cilexetil is unlikely to present a genotoxic hazard to humans under therapeutic conditions.

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