Bee venom genotoxicity on Saccharomyces cerevisiae cells - The role of mitochondria and YAP1 transcription factor

Toxicology. 2024 Mar:503:153768. doi: 10.1016/j.tox.2024.153768. Epub 2024 Mar 3.

Abstract

The present work aims to clarify the genotype differences of a model organism Saccharomyces cerevisiae in response to bee venom. The study evaluated various endpoints including cell survival, induction of physiologically active superoxide anions, mitotic gene conversion, mitotic crossing-over, reverse mutations, DNA double-strand breaks, and Ty1 retrotransposition. The role of the intact mitochondria and the YAP1 transcription factor was also evaluated. Our results indicate a genotype-specific response. The first experimental evidence has been provided that bee venom induces physiologically active superoxide anions and DNA double-strand breaks in S. cerevisiae. The lack of oxidative phosphorylation due to disrupted or missing mitochondrial DNA reduces but not diminishes the cytotoxicity of bee venom. The possible modes of action could be considered direct damage to membranes (cytotoxic effect) and indirect damage to DNA through oxidative stress (genotoxic effect). YAP1 transcription factor was not found to be directly involved in cell defense against bee venom treatment.

Keywords: Bee venom; DNA double-strand breaks; Ty1 retrotransposition; cytotoxicity; oxidative stress; reverse mutations.

MeSH terms

  • Bee Venoms* / toxicity
  • DNA / metabolism
  • DNA Damage
  • Humans
  • Mitochondria / metabolism
  • Saccharomyces cerevisiae Proteins* / genetics
  • Saccharomyces cerevisiae Proteins* / metabolism
  • Saccharomyces cerevisiae* / drug effects
  • Saccharomyces cerevisiae* / genetics
  • Superoxides / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism

Substances

  • Bee Venoms
  • DNA
  • Saccharomyces cerevisiae Proteins
  • Superoxides
  • Transcription Factors
  • YAP1 protein, S cerevisiae