Carcinogenesis, Vol 19, 1401-1407, Copyright © 1998 by Oxford University Press
VA Dubrovskaya and KE Wetterhahn
Intracellular metabolism of chromium(VI) [Cr(VI)] may lead to oxidative
stress and this may account for the ability of Cr(VI) to act as a complete
carcinogen. Therefore, we examined the effects of Cr(VI) treatment on the
expression of oxidative stress genes in normal human lung LL 24 cells and
human lung adenocarcinoma A549 cells. RT-PCR and northern blot analyses
were used to determine the steady-state mRNA levels of catalase,
glutathione S-transferase, glutathione reductase, Cu/Zn- and Mn-superoxide
dismutases, glutathione peroxidase, NAD(P)H:quinone oxidoreductase, heme
oxygenase and interleukin 8 in control cells and cells treated with 5-200
microM of Cr(VI). We found that only expression of the heme oxygenase gene
is strongly elevated under the treatment with Cr(VI), and only in normal
human lung LL 24 cells. Our data showed that even in the absence of Cr(VI)
treatment, the level of heme oxygenase gene expression is much higher in
A549 cells than in LL 24 cells. As glutathione is believed to play a
protective role in cells against different forms of oxidative stress, we
studied the correlation between intracellular glutathione levels and the
inducibility of the heme oxygenase gene after treatment of cells with
Cr(VI). Our results demonstrate that glutathione levels are increased by 35
% of control values in LL 24 cells treated with Cr(VI). The data obtained
indicate that heme oxygenase, known to be a stress- inducible gene, may be
involved in cellular pathways critical to the carcinogenic activity of
Cr(VI) in normal human lung cells. Intracellular glutathione levels and
reactive oxygen species do not appear to be primarily responsible for the
stress response, induced by Cr(VI) in the studied human cells.
ARTICLES
Effects of Cr(VI) on the expression of the oxidative stress genes in human lung cells
Department of Chemistry, Dartmouth College, Hanover, NH 03755-3564, USA.
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