Carcinogenesis, Vol 19, 2187-2193, Copyright © 1998 by Oxford University Press
J Chen, M Gokhale, Y Li, MA Trush and JD Yager
Ethinyl estradiol (EE) is a strong hepatic promoter and weak complete
hepatocarcinogen. Among the effects on rat liver caused by chronic exposure
to non-hepatotoxic doses of EE is an initial, transient increase in
hepatocyte growth followed by a subsequent inhibition (mitosuppression) of
basal and/or induced liver growth. To investigate the mechanism of
EE-induced mitosuppression, we performed a differential display and
identified 10 genes whose expression was increased 2- to 4-fold in
EE-induced, mitosuppressed livers (Chen et al., Carcinogenesis, 17,
2783-2786, 1996). We found that one of these clones was homologous to
nuclear genome-encoded mitochondrial ATP synthase subunit E. Here, we
describe the identification of two additional cDNAs representing
transcripts whose levels were elevated during EE-induced mitosuppression as
mitochondrial DNA-encoded cytochrome c oxidase subunit III and ATP synthase
6. In addition, we found that EE, estradiol and the estradiol catechol
metabolites, 4-OH- estradiol and 2-OH-estradiol, increased the levels of
these and other mitochondrial genome-encoded transcripts in human hepatoma
HepG2 cells. We also observed that this increase can be blocked by
inhibition of cytochrome P450-mediated estrogen metabolism, and that this
increase is accompanied by increased mitochondrial superoxide production,
which reflects increased respiratory chain activity.
ARTICLES
Enhanced levels of several mitochondrial mRNA transcripts and mitochondrial superoxide production during ethinyl estradiol-induced hepatocarcinogenesis and after estrogen treatment of HepG2 cells
Department of Environmental Health Sciences, Johns Hopkins School of Hygiene and Public Health, Baltimore, MD 21205-2179, USA.
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