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Lack of genotoxicity of piperonyl butoxide

W H Butler1, K L Gabriel, F J Preiss

  • 1BIBRA International, Carshalton, Surrey, UK.

Mutation Research
|December 20, 1996
PubMed

Insights

Piperonyl butoxide was not genotoxic in bacterial mutation assays or in mammalian cell assays. Liver tumors in rodents at high doses likely stem from a non-genotoxic mechanism, not DNA damage.

Area of Science:

  • Toxicology
  • Genetics
  • Biochemistry

Background:

  • Piperonyl butoxide is a common synergist used in pesticides.
  • Rodent studies have shown liver tumors at high doses of piperonyl butoxide.
  • The mechanism underlying tumor formation requires clarification.

Purpose of the Study:

  • To evaluate the genotoxicity of piperonyl butoxide.
  • To determine if piperonyl butoxide causes DNA damage or mutations.
  • To investigate the mechanism of liver tumor formation in rodents.

Main Methods:

  • Bacterial mutation assays (Ames test) with strains TA98, TA100, TA1535, TA1537, TA1538, with and without metabolic activation.
  • Mammalian cell assays: CHO/HGPRT mutation assay and chromosomal aberration assay in Chinese hamster ovary (CHO) cells, with and without metabolic activation.
  • In vitro unscheduled DNA synthesis (UDS) test using rat liver primary cell cultures.

Main Results:

  • Piperonyl butoxide did not induce mutations in bacterial assays.
  • No genotoxic effects were observed in the CHO/HGPRT or chromosomal aberration assays.
  • The in vitro UDS test showed no evidence of DNA damage.
  • Piperonyl butoxide was not genotoxic in any of the tested systems.

Conclusions:

  • Piperonyl butoxide does not exhibit genotoxic potential.
  • The liver tumors observed in rodents at high doses are likely due to a secondary, non-genotoxic mechanism.
  • These findings suggest piperonyl butoxide's safety profile is not linked to DNA damage.

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