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Role of catalase and oxidative stress in hepatic peroxisome proliferator‐induced morphological transformation of syrian hamster embryo cells
Author(s) -
Mikalsen SveinOle,
Kaalhus Olav,
Reith Albrecht,
Sanner Tore
Publication year - 1990
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910460533
Subject(s) - oxidative stress , peroxisome , catalase , phthalate , oxidative phosphorylation , chemistry , hamster , clofibrate , menadione , biochemistry , medicine , endocrinology , biology , organic chemistry , gene
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 H 2 O 2 ‐production from the strongly induced peroxisomal β‐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, coexposure 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 H 2 O 2 . Menadione only induced transformation at a toxic concentration, while H 2 O 2 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 H 2 O 2 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.