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Inhibition of thioredoxin reductase 1 by porphyrins and other small molecules identified by a high-throughput screening assay.
[erythropoietic protoporphyria]
The
selenoprotein
thioredoxin
reductase
1
(
TrxR
1
)
has
in
recent
years
been
identified
as
a
promising
anticancer
drug
target
.
A
high
-throughput
assay
for
discovery
of
novel
compounds
targeting
the
enzyme
is
therefore
warranted
.
Herein
,
we
describe
a
single
-enzyme
,
dual-purpose
assay
for
simultaneous
identification
of
inhibitors
and
substrates
of
TrxR
1
.
Using
this
assay
to
screen
the
LOPAC
¹²â¸â°
compound
collection
we
identified
several
known
inhibitors
of
TrxR
1
,
thus
validating
the
assay
,
as
well
as
several
compounds
hitherto
unknown
to
target
the
enzyme
.
These
included
rottlerin
(
previously
reported
as
a
PKCδ
inhibitor
and
mitochondrial
uncoupler
)
and
the
heme
precursor
protoporphyrin
IX
(
PpIX
)
.
We
found
that
PpIX
was
a
potent
competitive
inhibitor
of
TrxR
1
,
with
a
K
(
i
)
=
2
.
7
μM
with
regard
to
Trx
1
,
and
in
the
absence
of
Trx
1
displayed
time-dependent
irreversible
inhibition
with
an
apparent
second
-order
rate
constant
(
k
(
inact
)
)
of
(
0
.
73
±
0
.
07
)
×
10
â»
³
μM
â»
¹
min
â»
¹
.
Exogenously
delivered
PpIX
was
cytotoxic
,
inhibited
A
549
cell
proliferation
,
and
was
found
to
also
inhibit
cellular
TrxR
activity
.
Hemin
and
the
ferrochelatase
inhibitor
NMPP
also
inhibited
TrxR
1
and
showed
cytotoxicity
,
but
less
potently
compared
to
PpIX
.
We
conclude
that
rottlerin-induced
cellular
effects
may
involve
targeting
of
TrxR
1
.
The
unexpected
finding
of
PpIX
as
a
TrxR
1
inhibitor
suggests
that
such
inhibition
may
contribute
to
symptoms
associated
with
conditions
of
abnormally
high
PpIX
levels
,
such
as
reduced
ferrochelatase
activity
seen
in
erythropoietic
protoporphyria
.
Finally
,
additional
inhibitors
of
TrxR
1
may
be
discovered
and
further
characterized
based
upon
the
new
high
-throughput
TrxR
1
assay
presented
here
.
Diseases
Validation
Diseases presenting
"known inhibitors of"
symptom
erythropoietic protoporphyria
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