Antioxidants,
Journal Year:
2020,
Volume and Issue:
9(5), P. 383 - 383
Published: May 5, 2020
Selenium
is
a
vital
trace
element
present
as
selenocysteine
(Sec)
in
proteins
that
are,
thus,
known
selenoproteins.
Humans
have
25
selenoproteins,
most
of
which
are
functionally
characterized
oxidoreductases,
where
the
Sec
residue
plays
catalytic
role
redox
regulation
and
antioxidant
activity.
Glutathione
peroxidase
pivotal
scavenging
inactivating
hydrogen
lipid
peroxides,
whereas
thioredoxin
reductase
reduces
oxidized
thioredoxins
well
non-disulfide
substrates,
such
hydroperoxides
peroxide.
Selenoprotein
R
protects
cell
against
oxidative
damage
by
reducing
methionine-R-sulfoxide
back
to
methionine.
O
regulates
homeostasis
with
activity
protein
AMPylation.
Moreover,
endoplasmic
reticulum
(ER)
membrane
selenoproteins
(SelI,
K,
N,
S,
Sel15)
involved
ER
stress
regulation.
Selenoproteins
containing
CXXU
motif
(SelH,
M,
T,
V,
W)
putative
oxidoreductases
participate
various
cellular
processes
depending
on
Herein,
we
review
recent
studies
their
physiological
functions
humans,
diseases.
Frontiers in Physiology,
Journal Year:
2020,
Volume and Issue:
11
Published: July 2, 2020
Oxidative
stress
plays
an
essential
role
in
the
pathogenesis
of
chronic
diseases
such
as
cardiovascular
diseases,
diabetes,
neurodegenerative
and
cancer.
Long
term
exposure
to
increased
levels
pro-oxidant
factors
can
cause
structural
defects
at
a
mitochondrial
DNA
level,
well
functional
alteration
several
enzymes
cellular
structures
leading
aberrations
gene
expression.
The
modern
lifestyle
associated
with
processed
food,
wide
range
chemicals
lack
exercise
important
oxidative
induction.
However,
use
medicinal
plants
antioxidant
properties
has
been
exploited
for
their
ability
treat
or
prevent
human
pathologies
which
seems
be
one
causes.
In
this
review
we
discuss
is
triggers
plant-derived
compounds
mechanisms
defenses
that
help
prevention
these
diseases.
Finally,
both
beneficial
detrimental
effects
molecules
are
used
reduce
conditions
discussed.
Signal Transduction and Targeted Therapy,
Journal Year:
2021,
Volume and Issue:
6(1)
Published: Feb. 3, 2021
Abstract
Ferroptosis
is
an
iron-dependent
cell
death,
which
different
from
apoptosis,
necrosis,
autophagy,
and
other
forms
of
death.
The
process
ferroptotic
death
defined
by
the
accumulation
lethal
lipid
species
derived
peroxidation
lipids,
can
be
prevented
iron
chelators
(e.g.,
deferiprone,
deferoxamine)
small
lipophilic
antioxidants
ferrostatin,
liproxstatin).
This
review
summarizes
current
knowledge
about
regulatory
mechanism
ferroptosis
its
association
with
several
pathways,
including
iron,
lipid,
cysteine
metabolism.
We
have
further
discussed
contribution
to
pathogenesis
diseases
such
as
cancer,
ischemia/reperfusion,
various
neurodegenerative
Alzheimer’s
disease
Parkinson’s
disease),
evaluated
therapeutic
applications
inhibitors
in
clinics.
Cell Death and Differentiation,
Journal Year:
2019,
Volume and Issue:
26(11), P. 2284 - 2299
Published: Feb. 8, 2019
Ferroptosis
is
a
recently
identified
form
of
regulated
cell
death
defined
by
the
iron-dependent
accumulation
lipid
reactive
oxygen
species.
has
been
studied
in
various
diseases
such
as
cancer,
Parkinson's
disease,
and
stroke.
However,
exact
function
mechanism
ferroptosis
ischemia/reperfusion
(I/R)
injury,
especially
intestine,
remains
unknown.
Considering
unique
conditions
required
for
ferroptosis,
we
hypothesize
that
ischemia
promotes
immediately
after
intestinal
reperfusion.
In
contrast
to
conventional
strategies
employed
I/R
studies,
focused
on
ischemic
phase.
Here
verified
assessing
proferroptotic
changes
along
with
protein
peroxidation
levels
during
The
inhibition
liproxstatin-1
ameliorated
I/R-induced
injury.
Acyl-CoA
synthetase
long-chain
family
member
4
(ACSL4),
which
key
enzyme
regulates
composition,
shown
contribute
execution
but
its
role
needs
clarification.
present
study,
used
rosiglitazone
(ROSI)
siRNA
inhibit
ischemia/hypoxia-induced
ACSL4
vivo
vitro.
results
demonstrated
before
reperfusion
protected
against
death.
Further
investigation
revealed
special
1
(Sp1)
was
crucial
transcription
factor
increased
binding
promoter
region.
Collectively,
this
study
demonstrates
closely
associated
critical
lethal
process.
Sp1
an
important
promoting
expression.
These
suggest
effective
mechanistic
approach
injury
prevention
treatment.
Antioxidants and Redox Signaling,
Journal Year:
2017,
Volume and Issue:
29(1), P. 61 - 74
Published: May 2, 2017
Iron-dependent
lipid
peroxidation
is
a
complex
oxidative
process
where
phospholipid
hydroperoxides
(PLOOH)
are
produced
in
membranes
and
finally
transformed
into
series
of
decomposition
products,
some
which
endowed
with
biological
activity.
It
specifically
prevented
by
glutathione
peroxidase
4
(GPx4),
the
selenoenzyme
that
reduces
PLOOH
(GSH).
both
product
major
initiator
peroxidative
chain
reactions,
as
well
an
activator
lipoxygenases.
α-Tocopherol
breaks
propagation
inhibits
Thus,
GPx4,
GSH,
α-tocopherol
integrated
concerted
anti-peroxidant
mechanism.
Recent
Advances:
Ferroptosis
has
been
recently
identified
cell
death
subroutine
activated
missing
GPx4
activity
inhibited
iron
chelation
or
supplementation.
induction
may
underlie
spontaneous
human
diseases,
such
neurodegeneration
neuroinflammation,
causing
excessive
death.
The
basic
mechanism
ferroptosis,
therefore,
fits
features
activation
peroxidation.Still
lacking
convincing
proofs
lipoxygenases
involved
ferroptosis.
Also,
unknown
molecules
eventually
killing
cells
mechanisms
underlying
drop
cellular
capacity.Molecular
events
ferroptosis
to
be
unraveled
validated
on
animal
models
inactivation,
role
GSH
concentration,
increased
availability,
membrane
structure
composition.
This
expected
drive
drug
discovery
aimed
at
halting
degenerative
diseases
boosting
it
cancer
cells.
Antioxid.
Redox
Signal.
29,
61-74.
Genes & Development,
Journal Year:
2018,
Volume and Issue:
32(9-10), P. 602 - 619
Published: May 1, 2018
Lipid
peroxidation
is
the
process
by
which
oxygen
combines
with
lipids
to
generate
lipid
hydroperoxides
via
intermediate
formation
of
peroxyl
radicals.
Vitamin
E
and
coenzyme
Q
10
react
radicals
yield
peroxides,
then
these
oxidized
species
can
be
detoxified
glutathione
peroxidase
4
(GPX4)
other
components
cellular
antioxidant
defense
network.
Ferroptosis
a
form
regulated
nonapoptotic
cell
death
involving
overwhelming
iron-dependent
peroxidation.
Here,
we
review
functions
regulation
peroxidation,
ferroptosis,
network
in
diverse
species,
including
humans,
mammals
vertebrates,
plants,
invertebrates,
yeast,
bacteria,
archaea.
We
also
discuss
potential
evolutionary
roles
ferroptosis.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(3), P. 1009 - 1009
Published: Jan. 20, 2021
The
high
number
of
new
cancer
incidences
and
the
associated
mortality
continue
to
be
alarming,
leading
search
for
therapies
that
would
more
effective
less
burdensome
patients.
As
there
is
evidence
Se
compounds
can
have
chemopreventive
activity,
studies
begun
establish
whether
these
also
affect
already
existing
cancers.
This
review
aims
discuss
different
classes
Se-containing
compounds,
both
organic
inorganic,
natural
synthetic,
mechanisms
molecular
targets
their
anticancer
activity.
chemical
discussed
in
this
paper
include
inorganic
(selenite,
selenate)
such
as
diselenides,
selenides,
selenoesters,
methylseleninic
acid,
1,2-benzisoselenazole-3[2H]-one
selenophene-based
derivatives,
well
selenoamino
acids
Selol.
