Role of catalase and oxidative stress in hepatic peroxisome proliferator‐induced morphological transformation of Syrian hamster embryo cells

S.‐O. Mikalsen, O. Kaalhus, A. Reith, T. Sanner

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)

Abstract

Several hepatic peroxisome proliferators (HHPs) such as di(2-ethylhexyl)phthalate (DEHP), mono(2-ethylhexyl)-phthalate, clofibrate and tiadenol, induce morphological transformation of Syrian hamster embryo (SHE) cells in vitro. According to one hypothesis, the hepatocarcinogenic effect of HPPs is caused by an oxidative stress due to increased H2O2-production from the strongly induced peroxisomal beta-oxidation of fatty acids. Thus, increased transformation frequencies by HPPs should be obtained when catalase was inhibited by 3-amino-1,2,4-triazole (amitrole). However, co-exposure to HPPs and amitrole did not enhance the transformation frequencies for any of the HPPs. The sensitivity of SHE cells for oxidative agents was studied by using menadione and H2O2. Menadione only induced transformation at a toxic concentration, while H2O2 induced transformation at non-toxic concentrations. To study the generation of oxidative radicals in SHE cells, electron spin resonance was employed. No oxidative radical formation was detected in tiadenol- or DEHP-exposed SHE cells. When menadione or H2O2 were added during the measurements, oxidative radicals were found. A transmission electron microscopic study showed a small number of peroxisomes, and did not reveal any increase in the number of peroxisomes in clofibrate-treated SHE cells.
Original languageEnglish
Pages (from-to)950-957
Number of pages8
JournalInternational Journal of Cancer
Volume46
Issue number5
DOIs
Publication statusPublished - 1990
Externally publishedYes

Keywords

  • Peroxisome proliferators
  • oxidative stress
  • In vitro assays
  • Phthalates
  • DEHP
  • H2O2
  • Cell culture

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