International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(16), P. 12928 - 12928
Published: Aug. 18, 2023
Iron
is
essential
for
all
organisms
and
cells.
Diseases
of
iron
imbalance
affect
billions
patients,
including
those
with
overload
other
forms
toxicity.
Excess
load
an
adverse
prognostic
factor
diseases
can
cause
serious
organ
damage
fatalities
following
chronic
red
blood
cell
transfusions
in
patients
many
conditions,
hemoglobinopathies,
myelodyspasia,
hematopoietic
stem
transplantation.
Similar
toxicity
excess
body
but
at
a
slower
rate
disease
progression
found
idiopathic
haemochromatosis
patients.
deposition
different
regions
the
brain
suspected
has
been
identified
by
MRI
T2*
similar
methods
neurodegenerative
diseases,
Alzheimer’s
Parkinson’s
disease.
Based
on
its
role
as
major
biological
catalyst
free
radical
reactions
Fenton
reaction,
also
implicated
associated
pathology
tissue
damage.
Furthermore,
recent
discovery
ferroptosis,
which
death
program
based
generation
membrane
lipid
oxidation,
sparked
thousands
investigations
association
cardiac,
kidney,
liver,
cancer
infections.
The
implications
labile,
non-protein
bound
form
complexes
dietary
molecules
such
vitamin
C
drugs
doxorubicin
xenobiotic
relation
to
carcinogenesis
are
discussed.
In
each
case
toxicity,
mechanistic
insights,
diagnostic
criteria,
molecular
interactions
design
new
effective
therapeutic
interventions
future
targeted
strategies.
particular,
this
approach
successful
treatment
most
loading
conditions
especially
transition
thalassemia
from
fatal
due
protocols
resulting
complete
elimination
Food & Function,
Journal Year:
2024,
Volume and Issue:
15(7), P. 3411 - 3419
Published: Jan. 1, 2024
Tetrabromobisphenol
A
(TBBPA)
is
a
global
pollutant.
When
TBBPA
absorbed
by
the
body
through
various
routes,
it
can
have
wide
range
of
harmful
effects
on
body.
Green
tea
polyphenols
(GTPs)
act
as
antioxidants,
resisting
toxic
animals.
The
and
mechanisms
GTP
oxidative
stress,
inflammation
apoptosis
in
mouse
lung
are
unknown.
Therefore,
we
established
vivo
vitro
models
exposure
antagonism
using
C57
mice
A549
cells
examined
expression
factors
related
to
autophagy,
apoptosis.
results
study
showed
that
increase
reactive
oxygen
species
(ROS)
levels
after
decreased
autophagy-related
Beclin1,
LC3-II,
ATG3,
ATG5,
ATG7
ATG12
increased
p62;
stress
inhibits
autophagy
levels.
pro-inflammatory
IL-1β,
IL-6
TNF-α
anti-inflammatory
factor
IL-10
activation
NF-κB
p65/TNF-α
pathway.
Bax,
caspase-3,
caspase-7
caspase-9
Bcl-2
activate
apoptosis-related
pathways.
addition
attenuated
levels,
restored
inhibition
reduced
Our
suggest
attenuate
modulating
ROS,
reducing
increasing
attenuating
cells.
These
provide
fundamental
information
for
exploring
antioxidant
mechanism
further
studying
TBBPA.
Toxics,
Journal Year:
2025,
Volume and Issue:
13(2), P. 83 - 83
Published: Jan. 24, 2025
Prolonged
excessive
intake
of
fluoride
(F)
can
result
in
fluorosis,
leading
to
a
range
tissue
oxidative
damages.
Therefore,
mitigating
the
stress
induced
by
fluorosis
has
become
significant
research
concern.
Consequently,
how
relieve
caused
is
an
urgent
matter.
In
present
study,
intestinal
porcine
epithelial
(IPEC-J2)
cells
were
chosen
explore
underlying
mechanism
tea
polyphenols
(TPs)
on
F-induced
stress.
The
results
show
that
cytotoxicity
IPEC-J2
F
presented
dose-dependent
manner
according
cell
viability.
Additionally,
treatment
inhibited
activity
T-SOD,
CAT,
and
GSH-Px
as
well
their
transcription
levels,
increased
reactive
oxygen
(ROS)
formation
damage
rates,
then
promoted
apoptosis
through
TUNEL
mitochondrial
membrane
potential
detection
when
compared
with
from
control
group.
As
main
antioxidant
ingredient
tea,
TPs
alleviated
oxidation
via
blocking
ROS
generation
LDH’s
release,
promoting
tight
junction
(TJ)
proteins
activities
enzymes
cells.
These
provide
new
strategy
for
impairment.
Journal of Toxicology and Environmental Health,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 16
Published: Jan. 24, 2025
This
study
aimed
to
examine
the
dose-response
effects
of
polyphenon-60
derived
from
green
tea
(P60-GT)
on
hexavalent
chromium
[Cr(VI)]-induced
genotoxic
damage
and
apoptosis.
Male
Hsd:ICR
mice
were
divided
into
4
groups:
(1)
Control
(vehicle
only),
(2)
P60-GT
(15,
30,
or
45
mg/kg
gavage),
(3)
Cr(VI)
(20
CrO3
intraperitoneally),
(4)
P60-GT+CrO3
(P60-GT
administered
hr
before
CrO3).
Peripheral
blood
samples
collected
at
24,
48,
72
assess
number
micronuclei
(MN),
apoptosis,
cell
viability,
while
plasma
8-hydroxy-2'-deoxyguanosine
(8-OHdG)
levels
measured
0
48
hr.
significantly
increased
MN
frequency,
suppressed
8-OHdG
repair,
reduced
viability.
Pre-treatment
with
frequency
by
up
74%,
30
dose
demonstrating
highest
efficacy.
restored
enhanced
suggesting
activation
DNA
repair
apoptotic
pathways
as
potential
antigenotoxic
mechanisms.
The
15
exhibited
anti-apoptotic
effects,
doses
promoted
However,
resulted
in
100%
lethality
hr,
likely
due
synergistic
toxicity
Cr(VI).
These
findings
demonstrate
dose-dependent
protective
emphasize
need
for
dosage
optimization
maximize
therapeutic
benefits
minimizing
toxicity.
Toxicology Reports,
Journal Year:
2025,
Volume and Issue:
unknown, P. 101928 - 101928
Published: Jan. 1, 2025
Nedaplatin
has
demonstrated
remarkable
efficacy
in
combating
various
malignancies.
However,
the
administration
of
nedaplatin
been
associated
with
induction
DNA
damage
within
normal
cells.
Cilostazol
is
a
phosphodiesterase
III
inhibitor
an
antioxidant
mechanism
that
could
protect
cells
from
genotoxicity.
We
aimed
to
evaluate
genotoxic
effect
on
cultured
human
lymphocytes
and
potential
protective
cilostazol
chromosomal
induced
by
nedaplatin.
The
proposed
nedaplatin's
was
studied
vitro
evaluating
frequencies
sister
chromatid
exchanges
(SCEs)
lymphocytes.
Both
mitotic
proliferative
indices
(MI
PI,
respectively)
were
used
assess
cytotoxic
effects
significantly
increased
frequency
SCEs
compared
control
cilostazol-treated
injury
reduced
pretreatment
(P
<
0.0001).
Treating
alone
also
SCEs,
MI,
PI
group.
significant
decreases
MI
Pretreatment
partially
debilitated
nedaplatin-induced
changes
but
not
PI.
ameliorated
genotoxicity
Foods,
Journal Year:
2025,
Volume and Issue:
14(4), P. 679 - 679
Published: Feb. 17, 2025
Wilson’s
disease
(WD)
is
an
inherited
disorder
characterized
by
abnormal
copper
metabolism
with
complex
pathological
features.
Currently,
the
mechanism
of
overload-induced
hepatic
injury
unclear.
Green
tea
a
natural
chelator,
and
its
main
ingredients,
green
polyphenol
(GTP)
L-theanine
(L-TA)
are
good
at
binding
to
heavy
metals
like
iron
copper.
There
have
been
no
reports
on
extracts
(GTE)
for
treatment
disease.
This
study
investigated
hepatoprotective
effect
GTE
WD
model
mice.
Initially,
we
examined
impact
extract
metabolism,
excretion,
effects
in
toxic
milk
Then,
Ultra
performance
liquid
chromatography
(UPLC-DAD)
was
established
analyze
GTP
L-TA
extract.
Further
screening
eight
active
components
carried
out
ion
analyzer.
Finally,
verified
pharmacodynamic
these
ingredients
animal
level.
The
results
showed
that
improves
liver
function
attenuates
TX
mice
promoting
tissue
excretion
inhibiting
oxidative
stress,
which
provides
theoretical
basis
tea’s
potential
improve
clinical
symptoms
WD.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
14(1), P. 29 - 29
Published: Dec. 29, 2024
Epidemiological
studies
have
suggested
that
following
long-term,
low-dose
daily
aspirin
(LTLDA)
administration
for
more
than
5
years
at
75–100
mg/day,
20–30%
of
patients
(50–80
old)
had
a
lower
risk
developing
colorectal
cancer
(CRC)
and
about
the
same
proportion
in
iron
deficiency
anemia
(IDA).
In
cases
IDA,
an
increase
excretion
is
suspected,
which
caused
by
chelating
metabolites
(ACMs):
salicylic
acid,
salicyluric
2,5-dihydroxybenzoic
2,3-dihydroxybenzoic
acid.
The
ACMs
constitute
70%
administered
dose
much
longer
half-lives
blood
tissues.
mechanisms
reduction
LTLDA
users
likely
due
to
ACM’s
targeting
involved
free
radical
damage,
iron-containing
toxins,
proteins,
associated
metabolic
pathways
such
as
ferroptosis.
from
non-absorbed
(about
30%)
may
also
mitigate
toxicity
heme
nitroso-heme
other
toxins
food,
are
responsible
cause
cancer.
mode
action
antioxidant
pro-drug
ACMs,
with
continuous
presence
users,
increases
prospect
prophylaxis
diseases.
It
anticancer
effects
depend
primarily
on
iron-chelating
activity
ACMs.
role
diseases
incomplete
without
considering
its
rapid
biotransformation
half-life
