Biomeditsinskaya Khimiya,
Journal Year:
2023,
Volume and Issue:
69(2), P. 83 - 96
Published: Jan. 1, 2023
The
review
considers
molecular
mechanisms
underlying
formation
and
development
of
oxidative
stress
(OS)
in
patients
with
alcohol
dependence.
major
attention
is
paid
to
the
effects
ethanol
its
metabolite
acetaldehyde
associated
additional
sources
generation
reactive
oxygen
species
(ROS)
response
exogenous
ethanol.
own
results
studies
vitro
effect
on
concentration
peripheral
OS
markers
—
products
modification
proteins
(protein
carbonyls),
lipids
(lipid
peroxidation
products),
DNA
(8-hydroxy-2-deoxyguanosine,
8-OHdG)
blood
plasma
are
presented.
changes
these
parameters
activity
antioxidant
enzymes
(SOD,
catalase)
dependence
were
analyzed.
Own
literature
data
indicate
that
at
a
certain
stage
disease
can
play
protective
rather
than
pathogenic
role
body.
Antioxidants,
Journal Year:
2021,
Volume and Issue:
10(9), P. 1419 - 1419
Published: Sept. 5, 2021
Reactive
oxygen
species
(ROS)
are
noxious
to
cells
because
their
increased
level
interacts
with
the
body’s
defense
mechanism.
These
also
cause
mutations
and
uncontrolled
cell
division,
resulting
in
oxidative
stress
(OS).
Prolonged
is
responsible
for
incorrect
protein
folding
endoplasmic
reticulum
(ER),
causing
a
stressful
condition,
ER
stress.
cellular
stresses
(oxidative
stress)
well-recognized
biological
factors
that
play
prominent
role
progression
of
hepatocellular
carcinoma
(HCC).
HCC
critical
global
health
problem
third
leading
cancer-related
mortality.
The
application
anti-oxidants
from
herbal
sources
significantly
reduces
Kaempferol
(KP)
naturally
occurring,
aglycone
dietary
flavonoid
present
various
plants
(Crocus
sativus,
Coccinia
grandis,
Euphorbia
pekinensis,
varieties
Aloe
vera,
etc.)
It
capable
interacting
pleiotropic
proteins
human
body.
Efforts
progress
develop
KP
as
potential
candidate
prevent
no
adverse
effects.
This
review
emphasizes
molecular
mechanism
treating
HCC,
targeting
Biomedicines,
Journal Year:
2021,
Volume and Issue:
9(6), P. 687 - 687
Published: June 17, 2021
A
peculiar
role
for
oxidative
stress
in
non-alcoholic
fatty
liver
disease
(NAFLD)
and
its
transition
to
the
inflammatory
complication
steatohepatitis
(NASH),
as
well
threatening
evolution
hepatocellular
carcinoma
(HCC),
is
supported
by
numerous
experimental
clinical
studies.
NADPH
oxidases
(NOXs)
are
enzymes
producing
reactive
oxygen
species
(ROS),
whose
abundance
cells
closely
related
inflammation
immune
responses.
Here,
we
reviewed
recent
findings
regarding
this
topic,
focusing
on
of
NOXs
different
stages
describing
current
knowledge
about
their
mechanisms
action.
We
conclude
that,
although
there
a
consensus
that
NOX-produced
ROS
toxic
non-neoplastic
conditions
due
vicious
cycle
sustaining
NAFLD
NASH,
effect
controversial
neoplastic
towards
HCC.
In
regard,
indications
differential
NOX
isoforms,
since
NOX1
NOX2
play
detrimental
role,
whereas
increased
NOX4
expression
appears
be
correlated
with
better
HCC
prognosis
some
Further
studies
needed
fully
unravel
action
relationships
signaling
pathways
modulating
steatosis
cancer
development.
Livers,
Journal Year:
2022,
Volume and Issue:
2(1), P. 30 - 76
Published: Feb. 1, 2022
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
a
challenging
caused
by
multiple
factors,
which
may
partly
explain
why
it
still
remains
an
orphan
of
adequate
therapies.
This
review
highlights
the
interaction
between
oxidative
stress
(OS)
and
disturbed
lipid
metabolism.
Several
reactive
oxygen
species
generators,
including
those
produced
in
gastrointestinal
tract,
contribute
to
lipotoxic
hepatic
(and
extrahepatic)
damage
acids
great
variety
their
biologically
active
metabolites
“multiple
parallel-hit
model”.
leads
inflammation
fibrogenesis
contributes
NAFLD
progression.
The
alterations
oxidant/antioxidant
balance
affect
also
metabolism-related
organelles,
leading
peroxidation,
mitochondrial
dysfunction,
endoplasmic
reticulum
stress.
OS-induced
at
least
partially
counteracted
physiological
antioxidant
response.
Therefore,
modulation
this
defense
system
emerges
as
interesting
target
prevent
development
For
instance,
probiotics,
prebiotics,
diet,
fecal
microbiota
transplantation
represent
new
therapeutic
approaches
targeting
gut
dysbiosis.
OS
its
counter-regulation
are
under
influence
individual
genetic
epigenetic
factors
well.
In
near
future,
precision
medicine
taking
into
consideration
or
environmental
risk
coupled
with
biomarkers,
will
likely
assist
noninvasive
diagnosis
monitoring
progression
further
personalizing
treatments.
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(11), P. 1928 - 1928
Published: Oct. 29, 2023
Chronic
liver
disease
(CLD)
affects
a
significant
portion
of
the
global
population,
leading
to
substantial
number
deaths
each
year.
Distinct
forms
like
non-alcoholic
fatty
(NAFLD)
and
alcoholic
(ALD),
though
they
have
different
etiologies,
highlight
shared
pathologies
rooted
in
oxidative
stress.
Central
metabolism,
mitochondria
are
essential
for
ATP
production,
gluconeogenesis,
acid
oxidation,
heme
synthesis.
However,
diseases
NAFLD,
ALD,
fibrosis,
mitochondrial
function
is
compromised
by
inflammatory
cytokines,
hepatotoxins,
metabolic
irregularities.
This
dysfunction,
especially
electron
leakage,
exacerbates
production
reactive
oxygen
species
(ROS),
augmenting
damage.
Amidst
this,
nuclear
factor
erythroid
2-related
2
(NRF2)
emerges
as
cellular
protector.
It
not
only
counters
stress
regulating
antioxidant
genes
but
also
maintains
health
overseeing
autophagy
biogenesis.
The
synergy
between
NRF2
modulation
introduces
new
therapeutic
potentials
CLD,
focusing
on
preserving
integrity
against
threats.
review
delves
into
intricate
role
shedding
light
innovative
strategies
its
prevention
treatment,
through
pathways.
Frontiers in Pharmacology,
Journal Year:
2021,
Volume and Issue:
12
Published: Nov. 15, 2021
As
a
natural
active
substance,
dihydromyricetin
(DHM)
has
been
proven
to
have
good
hepatoprotective
activity.
However,
the
therapeutic
effect
of
DHM
on
liver
fibrosis,
which
become
disease
threatening
health
people
around
world,
not
studied
date.
The
purpose
this
study
was
investigate
as
new
nutritional
supplement
thioacetamide
(TAA)-induced
fibrosis.
fibrosis
model
established
by
intraperitoneal
injection
TAA
(200
mg/kg,
every
3
days)
for
8
weeks,
and
oral
administration
(20
mg/kg
40
daily)
after
4
weeks
TAA-induced
results
showed
that
treatment
significantly
inhibited
activities
alanine
aminotransferase
(ALT)
(37.81
±
7.62
U/L)
aspartate
(AST)
(55.18
10.94
in
serum
mice,
increased
levels
superoxide
dismutase
(SOD)
glutathione
(GSH)
while
reversed
level
malondialdehyde
(MDA).
In
addition,
histopathological
examination
illustrated
induced
inflammatory
infiltration,
apoptosis
fibroatherosclerotic
deposition
liver,
further
confirmed
western-blot
immunofluorescence
staining.
Moreover,
hepatocyte
regulating
phosphorylation
phosphatidylinositol
3-kinase
(PI3K),
protein
kinase-B
(AKT)
its
downstream
apoptotic
family.
Interestingly,
staining
alpha
smooth
muscle
actin
(α-SMA),
marker
hepatic
stellate
cell
activation,
regulated
expression
transforming
growth
factor
(TGF-β1).
Importantly,
supplementation
with
release
nuclear
kappa-B
(NF-κB)
signaling
pathway
pro-inflammatory
factors
tissue
TAA,
improved
fiber
diseases,
such
tumor
necrosis
(TNF-α)
recombinant
rat
IL-1β
(IL-1β).
conclusion,
evidence
revealed
is
potential
factor,
also
provides
possibility
Cancers,
Journal Year:
2023,
Volume and Issue:
15(3), P. 729 - 729
Published: Jan. 25, 2023
Within
the
aging
population,
frequency
of
cancer
is
increasing
dramatically.
In
addition,
multiple
genetic
and
environmental
factors
lead
to
common
multifactorial
diseases,
including
cardiovascular
disease,
chronic
kidney
obstructive
pulmonary
metabolic-associated
fatty
liver
disease.
recent
years,
there
has
been
a
growing
awareness
connection
between
as
well
how
one
can
affect
other,
resulting
in
vicious
cycle.
Although
exact
mechanistic
explanations
behind
this
remain
be
fully
explored,
some
progress
made
uncovering
pathologic
mechanisms.
review,
we
focus
on
nature
link
conditions,
specific
shared
mechanisms,
which
may
represent
either
preventive
or
therapeutic
targets.
Rather
than
organ-specific
interactions,
herein
mechanisms
among
explain
increased
risk.
More
research
subject
will
highlight
significance
developing
new
drugs
that
target
systems
rather
just
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(2), P. 212 - 212
Published: Feb. 8, 2024
(1)
Background:
Ozone
exposure
is
a
promising
tool
for
treating
liver
damage
since
it
known
to
control
the
release
of
free
radicals
and
increase
expression
antioxidant
enzymes.
The
objective
investigate
main
intracellular
pathways
activated
after
ozone,
considering
dosage
enzymes
markers
oxidative
stress.
(2)
Methods:
This
systematic
review
was
performed
based
on
PRISMA
guidelines
using
structured
search
in
MEDLINE
(PubMed),
Scopus,
Web
Science.
Bias
analysis
methodological
quality
assessments
were
examined
SYRCLE
Risk
tool.
(3)
Results:
Nineteen
studies
selected.
results
showed
that
ozone
has
protective
effect
tissue,
promoting
decrease
inflammatory
reduction
stress
tissue.
In
addition,
also
promoted
an
morphological
consequences
controlling
these
reducing
tissue
process
areas
degeneration
necrosis.
(4)
Conclusions:
beneficial
models
injury
through
markers.
regulates
Nrf2/ARE
pathway
blocks
NF-κB
pathway.
Toxicology Reports,
Journal Year:
2025,
Volume and Issue:
14, P. 101988 - 101988
Published: March 12, 2025
Methoxychlor
(MXC),
a
widely
used
pesticide,
poses
significant
toxicological
risks
to
various
biological
systems.
It
is
an
environmental
contaminant
and
the
only
organochlorine
pesticide
still
using
instead
of
DDT.
Endocrine
disruption
MXC
also
under
investigation.This
study
aimed
investigate
effects
on
antioxidant
status,
lipid
peroxidation,
liver
metabolism
in
experimental
rats.
Male
Wistar
rats
were
divided
into
control
treatment
groups,
with
latter
receiving
150
mg/kg
250
body
weight
(BW)
via
oral
administration
for
30
days.
Liver
function
was
assessed
by
measuring
circulating
biomarkers,
including
Alanine
Transaminase
(ALT),
Aspartate
(AST),
Alkaline
Phosphatase
(ALP).
Oxidative
damage
evaluated
determining
Thiobarbituric
Acid
Reactive
Substances
(TBARS),
hydroperoxide
(HYP),
other
peroxidation
markers.
Key
enzymes
involved
defense
mechanisms
analyzed
animals.
Our
results
demonstrated
increase
ALT,
AST,
ALP
levels
serum
exposed
MXC,
indicating
impaired
function.
This
accompanied
elevated
further
emphasizing
oxidative
stress.
Moreover,
activities
such
as
SOD,
GPx,
CAT
markedly
reduced
MXC-exposed
groups
compared
controls,
suggesting
compromised
system.
These
findings
suggest
that
methoxychlor
exposure
disrupts
induces
stress
enhancing
thereby
depleting
natural
defenses.
highlights
potential
hepatotoxic
underscores
role
mediating
its
toxicity.