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.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(19), P. 7152 - 7152
Published: Sept. 28, 2020
The
brain
is
vulnerable
to
excessive
oxidative
insults
because
of
its
abundant
lipid
content,
high
energy
requirements,
and
weak
antioxidant
capacity.
Reactive
oxygen
species
(ROS)
increase
susceptibility
neuronal
damage
functional
deficits,
via
changes
in
the
neurodegenerative
diseases.
Overabundance
abnormal
levels
ROS
and/or
overload
metals
are
regulated
by
cellular
defense
mechanisms,
intracellular
signaling,
physiological
functions
antioxidants
brain.
Single
complex
compounds
targeting
stress,
redox
metals,
cell
death
have
been
evaluated
multiple
preclinical
clinical
trials
as
a
complementary
therapeutic
strategy
for
combating
stress
associated
with
Herein,
we
present
general
analysis
overview
various
suggest
potential
courses
treatments
neuroprotection
from
injury.
This
review
focuses
on
enzymatic
non-enzymatic
mechanisms
examines
relative
advantages
methodological
concerns
when
assessing
treatment
disorders.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(22), P. 8765 - 8765
Published: Nov. 20, 2020
Ferroptosis
is
a
type
of
cell
death
that
was
described
less
than
decade
ago.
It
caused
by
the
excess
free
intracellular
iron
leads
to
lipid
(hydro)
peroxidation.
Iron
essential
as
redox
metal
in
several
physiological
functions.
The
brain
one
organs
known
be
affected
homeostatic
balance
disruption.
Since
1960s,
increased
concentration
central
nervous
system
has
been
associated
with
oxidative
stress,
oxidation
proteins
and
lipids,
death.
Here,
we
review
main
mechanisms
involved
process
ferroptosis
such
peroxidation,
glutathione
peroxidase
4
enzyme
activity,
metabolism.
Moreover,
association
pathophysiology
some
neurodegenerative
diseases,
namely
Alzheimer’s,
Parkinson’s,
Huntington’s
also
addressed.
Cell chemical biology,
Journal Year:
2020,
Volume and Issue:
27(4), P. 436 - 447
Published: April 1, 2020
Ferroptosis
is
a
non-apoptotic
mode
of
regulated
cell
death
that
iron
and
lipid
peroxidation
dependent.
As
new
mechanistic
insight
into
ferroptotic
effectors
how
they
are
in
different
disease
contexts
uncovered,
our
understanding
the
physiological
pathological
relevance
this
continues
to
grow.
Along
these
lines,
host
pharmacological
modulators
pathway
have
been
identified,
targeting
proteins
involved
homeostasis;
generation
reduction
peroxides;
or
cystine
import
glutathione
metabolism.
Also,
note,
many
components
ferroptosis
cascade
target
genes
transcription
factor
nuclear
erythroid
2-related
2
(NRF2),
indicating
its
critical
role
mediating
response.
In
review,
we
discuss
vitro,
vivo,
clinical
evidence
disease,
including
brief
discussion
upstream
mediators
cascade,
NRF2,
treat
ferroptosis-driven
diseases.
Journal of Cellular Physiology,
Journal Year:
2018,
Volume and Issue:
233(12), P. 9179 - 9190
Published: Aug. 4, 2018
Nuclear
receptor
coactivator
4
mediated
ferritinophagy
is
an
autophagic
phenomenon
that
specifically
involves
ferritin
to
release
intracellular
free
iron.
Ferritinophagy
implicated
in
maintaining
efficient
erythropoiesis.
Notably,
also
plays
a
central
role
driving
some
pathological
processes,
including
Parkinson's
disease
(PD)
and
urinary
tract
infections.
Some
evidence
has
demonstrated
critical
induce
ferroptosis.
Ferroptosis
newly
nonapoptotic
form
of
cell
death,
characterized
by
the
accumulation
iron-based
lipid
reactive
oxygen
species.
important
inhibiting
types
cancers,
such
as
hepatocellular
carcinoma,
pancreatic
prostate
cancer,
breast
cancer.
Conversely,
activation
ferroptosis
accelerates
neurodegeneration
diseases,
PD
Alzheimer's
disease.
Therefore,
this
review,
we
summarize
regulatory
mechanisms
related
Moreover,
distinctive
effects
human
erythropoiesis
pathologies,
coupled
with
promotive
or
inhibitory
tumorous
neurodegenerative
diseases
ferroptosis,
are
elucidated.
Obviously,
activating
could
be
exploited
achieve
desirable
therapeutic
on
diverse
cancers
diseases.
Interrupting
control
iron
level
might
provide
potentially
avenue
suppress
Journal of Biological Chemistry,
Journal Year:
2020,
Volume and Issue:
296, P. 100105 - 100105
Published: Nov. 20, 2020
Treatments
for
Alzheimer's
disease
(AD)
directed
against
the
prominent
amyloid
plaque
neuropathology
are
yet
to
be
proved
effective
despite
many
phase
3
clinical
trials.
There
several
other
neurochemical
abnormalities
that
occur
in
AD
brain
warrant
renewed
emphasis
as
potential
therapeutic
targets
this
disease.
Among
those
elementomic
signatures
of
iron,
copper,
zinc,
and
selenium.
Here,
we
review
these
essential
elements
their
broad
contribute
pathophysiology,
also
highlight
more
recent
attempts
translate
findings
into
therapeutics.
A
reinspection
large
bodies
discovery
field,
such
this,
may
inspire
new
thinking
about
pathogenesis
targets.
Frontiers in Pharmacology,
Journal Year:
2022,
Volume and Issue:
13
Published: Aug. 29, 2022
The
activation
of
ferroptosis
is
a
new
effective
way
to
treat
drug-resistant
solid
tumors.
Ferroptosis
an
iron-mediated
form
cell
death
caused
by
the
accumulation
lipid
peroxides.
intracellular
imbalance
between
oxidant
and
antioxidant
due
abnormal
expression
multiple
redox
active
enzymes
will
promote
produce
reactive
oxygen
species
(ROS).
So
far,
few
pathways
regulators
have
been
discovered
regulate
ferroptosis.
In
particular,
cystine/glutamate
antiporter
(System
X
c
−
),
glutathione
peroxidase
4
(GPX4)
(GSH)
/GSH/GPX4
axis)
plays
key
role
in
preventing
peroxidation-mediated
ferroptosis,
because
which
could
be
inhibited
blocking
System
axis.
This
review
aims
present
current
understanding
mechanism
based
on
axis
treatment
