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Irradiation induces the production of superoxide radicals (O),
which play an important causative role in radiation damage. Manganese
superoxide dismutase (MnSOD) is a mitochondrial enzyme involved in
scavenging O. This study examined MnSOD gene regulation by irradiation
in WI38 human fibroblasts. Unstimulated fibroblasts constitutively
expressed MnSOD activity and mRNA; irradiation markedly increased MnSOD
activity and mRNA levels. The increase in MnSOD transcripts by
irradiation was both time- and dose-dependent. WI38 fibroblasts
constitutively produce low levels of interleukin-1 (IL-1). The
induction of MnSOD mRNA by irradiation was partially blocked by
anti-IL-1 antibodies, and treatment of cells with IL-1 also increased
MnSOD mRNA levels. Inhibition of the cyclo-oxygenase pathway with
indomethacin augmented the induction MnSOD mRNA by irradiation and
prostaglandin E
Volume 270,
Number 26,
Issue of June 30, pp. 15864-15869, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
POSSIBLE MECHANISMS FOR ITS ACCUMULATION
inhibited the accumulation of MnSOD mRNA by
irradiation. Transcriptional run-on analysis showed that irradiation
increased the rate of MnSOD transcription 2-fold. Stability studies of
MnSOD mRNA in these cells showed that the half-life increased from
<1.5 h in unirradiated cells to >4 h in irradiated cells. These
results suggest that induction of the MnSOD gene after irradiation is
regulated, at least in part, by IL-1 production and that increased
levels of MnSOD transcripts also occur through a pathway of endogenous
prostaglandin E production. Our data indicate that the
increase in MnSOD mRNA observed after irradiation occurs through both
transcriptional and post-transcriptional mechanisms.
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