Antioxidants,
Journal Year:
2022,
Volume and Issue:
11(6), P. 1128 - 1128
Published: June 8, 2022
Cancer
is
characterized
by
increased
oxidative
stress,
an
imbalance
between
reactive
oxygen
species
(ROS)
and
antioxidants.
Enhanced
ROS
accumulation,
as
a
result
of
metabolic
disturbances
signaling
aberrations,
can
promote
carcinogenesis
malignant
progression
inducing
gene
mutations
activating
pro-oncogenic
signaling,
providing
possible
rationale
for
targeting
stress
in
cancer
treatment.
While
numerous
antioxidants
have
demonstrated
therapeutic
potential,
their
clinical
efficacy
remains
unproven.
Here,
we
review
the
for,
recent
advances
in,
pre-clinical
research
on
antioxidant
therapy
cancer,
including
with
nonenzymatic
antioxidants,
such
NRF2
activators,
vitamins,
N-acetylcysteine
GSH
esters,
or
enzymatic
NOX
inhibitors
SOD
mimics.
In
addition,
will
offer
insights
into
prospective
options
improving
effectiveness
therapy,
which
may
expand
its
applications
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(9), P. 4642 - 4642
Published: April 28, 2021
Living
species
are
continuously
subjected
to
all
extrinsic
forms
of
reactive
oxidants
and
others
that
produced
endogenously.
There
is
extensive
literature
on
the
generation
effects
oxygen
(ROS)
in
biological
processes,
both
terms
alteration
their
role
cellular
signaling
regulatory
pathways.
Cells
produce
ROS
as
a
controlled
physiological
process,
but
increasing
becomes
pathological
leads
oxidative
stress
disease.
The
induction
an
imbalance
between
production
radical
antioxidant
defense
systems,
which
can
cause
damage
biomolecules,
including
lipids,
proteins
DNA.
Cellular
biochemical
experiments
have
been
complemented
various
ways
explain
chemistry
oxidants.
However,
it
often
unclear
how
this
translates
into
chemical
reactions
involving
redox
changes.
This
review
addresses
question
includes
robust
mechanistic
explanation
stress.
Archives of Toxicology,
Journal Year:
2023,
Volume and Issue:
97(10), P. 2499 - 2574
Published: Aug. 19, 2023
Abstract
A
physiological
level
of
oxygen/nitrogen
free
radicals
and
non-radical
reactive
species
(collectively
known
as
ROS/RNS)
is
termed
oxidative
eustress
or
“good
stress”
characterized
by
low
to
mild
levels
oxidants
involved
in
the
regulation
various
biochemical
transformations
such
carboxylation,
hydroxylation,
peroxidation,
modulation
signal
transduction
pathways
Nuclear
factor-κB
(NF-κB),
Mitogen-activated
protein
kinase
(MAPK)
cascade,
phosphoinositide-3-kinase,
nuclear
factor
erythroid
2–related
2
(Nrf2)
other
processes.
Increased
ROS/RNS,
generated
from
both
endogenous
(mitochondria,
NADPH
oxidases)
and/or
exogenous
sources
(radiation,
certain
drugs,
foods,
cigarette
smoking,
pollution)
result
a
harmful
condition
stress
(“bad
stress”).
Although
it
widely
accepted,
that
many
chronic
diseases
are
multifactorial
origin,
they
share
common
denominator.
Here
we
review
importance
mechanisms
through
which
contributes
pathological
states
an
organism.
Attention
focused
on
chemistry
ROS
RNS
(e.g.
superoxide
radical,
hydrogen
peroxide,
hydroxyl
radicals,
peroxyl
nitric
oxide,
peroxynitrite),
their
role
damage
DNA,
proteins,
membrane
lipids.
Quantitative
qualitative
assessment
biomarkers
also
discussed.
Oxidative
pathology
cancer,
cardiovascular
diseases,
diabetes,
neurological
disorders
(Alzheimer’s
Parkinson’s
Down
syndrome),
psychiatric
(depression,
schizophrenia,
bipolar
disorder),
renal
disease,
lung
disease
(chronic
pulmonary
obstruction,
cancer),
aging.
The
concerted
action
antioxidants
ameliorate
effect
achieved
antioxidant
enzymes
(Superoxide
dismutases-SODs,
catalase,
glutathione
peroxidase-GPx),
small
molecular
weight
(vitamins
C
E,
flavonoids,
carotenoids,
melatonin,
ergothioneine,
others).
Perhaps
one
most
effective
vitamin
first
line
defense
against
peroxidation
promising
approach
appears
be
use
flavonoids),
showing
weak
prooxidant
properties
may
boost
cellular
systems
thus
act
preventive
anticancer
agents.
Redox
metal-based
enzyme
mimetic
compounds
potential
pharmaceutical
interventions
sirtuins
therapeutic
targets
for
age-related
anti-aging
strategies
Theranostics,
Journal Year:
2021,
Volume and Issue:
11(10), P. 4839 - 4857
Published: Jan. 1, 2021
Reactive
oxygen
species
(ROS)
serve
as
cell
signaling
molecules
generated
in
oxidative
metabolism
and
are
associated
with
a
number
of
human
diseases.
The
reprogramming
redox
induces
abnormal
accumulation
ROS
cancer
cells.
It
has
been
widely
accepted
that
play
opposite
roles
tumor
growth,
metastasis
apoptosis
according
to
their
different
distributions,
concentrations
durations
specific
subcellular
structures.
These
double-edged
progression
include
the
ROS-dependent
malignant
transformation
stress-induced
death.
In
this
review,
we
summarize
notable
literatures
on
generation
scavenging,
discuss
related
signal
transduction
networks
corresponding
anticancer
therapies.
There
is
no
doubt
an
improved
understanding
sophisticated
mechanism
biology
imperative
conquer
cancer.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(7), P. 3765 - 3765
Published: April 5, 2021
Anti-angiogenic
therapy
is
an
old
method
to
fight
cancer
that
aims
abolish
the
nutrient
and
oxygen
supply
tumor
cells
through
decrease
of
vascular
network
avoidance
new
blood
vessels
formation.
Most
anti-angiogenic
agents
approved
for
treatment
rely
on
targeting
endothelial
growth
factor
(VEGF)
actions,
as
VEGF
signaling
considered
main
angiogenesis
promotor.
In
addition
control
angiogenesis,
these
drugs
can
potentiate
immune
also
exhibits
immunosuppressive
functions.
Despite
mechanistic
rational
strongly
supports
benefit
stop
progression,
they
revealed
be
insufficient
in
most
cases.
We
hypothesize
rehabilitation
interfere
with
mechanisms
related
microenvironment
might
represent
a
promising
strategy.
this
review,
we
deepened
research
molecular
underlying
strategies
their
failure
went
further
into
alternative
impact
angiogenesis.
concluded
combinatory
effectors
angiogenic
pathways
putative
solution
therapies.
Advanced Science,
Journal Year:
2021,
Volume and Issue:
9(1)
Published: Nov. 19, 2021
Abstract
The
past
decades
have
witnessed
great
progress
in
cancer
immunotherapy,
which
has
profoundly
revolutionized
oncology,
whereas
low
patient
response
rates
and
potential
immune‐related
adverse
events
remain
major
clinical
challenges.
With
the
advantages
of
controlled
delivery
modular
flexibility,
nanomedicine
offered
opportunities
to
strengthen
antitumor
immune
responses
sensitize
tumor
immunotherapy.
Furthermore,
tumor‐microenvironment
(TME)‐responsive
been
demonstrated
achieve
specific
localized
amplification
tissue
a
safe
effective
manner,
increasing
immunotherapy
reducing
side
effects
simultaneously.
Here,
recent
TME‐responsive
for
is
summarized,
responds
signals
TME,
such
as
weak
acidity,
reductive
environment,
high‐level
reactive
oxygen
species,
hypoxia,
overexpressed
enzymes,
adenosine
triphosphate.
Moreover,
combine
nanomedicine‐based
therapy
immunotherapeutic
strategies
overcome
each
step
cancer‐immunity
cycle
enhance
discussed.
Finally,
existing
challenges
further
perspectives
this
rising
field
with
hope
improved
development
applications
are
Cells,
Journal Year:
2019,
Volume and Issue:
8(9), P. 1105 - 1105
Published: Sept. 18, 2019
Radiotherapy
is
one
of
the
major
cancer
treatment
strategies.
Exposure
to
penetrating
radiation
causes
cellular
stress,
directly
or
indirectly,
due
generation
reactive
oxygen
species,
DNA
damage,
and
subcellular
organelle
damage
autophagy.
These
radiation-induced
responses
cooperatively
contribute
cell
death,
but
paradoxically,
radiotherapy
also
activation
damage-repair
survival
signaling
alleviate
cytotoxic
effects
in
a
small
percentage
cells,
these
activations
are
responsible
for
tumor
radio-resistance.
The
present
study
describes
molecular
mechanisms
stress
response
radioresistance,
therapeutic
approaches
used
overcome
radioresistance.
Cancers,
Journal Year:
2020,
Volume and Issue:
12(4), P. 1050 - 1050
Published: April 23, 2020
DNA
damage
is
well
recognized
as
a
critical
factor
in
cancer
development
and
progression.
lesions
create
an
abnormal
nucleotide
or
fragment,
causing
break
one
both
chains
of
the
strand.
When
occurs,
possibility
generated
mutations
increases.
Genomic
instability
most
important
factors
that
lead
to
development.
repair
pathways
perform
essential
role
correcting
occur
from
damaging
agents
carcinogens,
thus
maintaining
genomic
stability.
Inefficient
driving
force
behind
establishment,
progression
evolution.
A
thorough
understanding
mechanisms
will
allow
for
better
therapeutic
intervention.
In
this
review
we
discuss
relationship
between
damage/repair
cancer,
how
can
target
these
pathways.