Journal of Agricultural and Food Chemistry,
Journal Year:
2023,
Volume and Issue:
71(31), P. 12043 - 12051
Published: July 20, 2023
Cadmium
is
highly
toxic
and
present
in
the
environment
can
be
accumulated
among
various
levels
of
food
chain.
Both
humans
animals
are
at
risk
from
toxicity
associated
with
cadmium.
However,
neurological
endpoint
caused
by
cadmium
has
not
been
revealed.
The
aim
our
research
to
explore
potential
target
attack
when
causing
neurotoxicity.
80
male
chickens
(one
day
old,
weighing
36.49
±
2.88
g)
were
randomly
divided
into
four
groups
independently
treated
0,
35,
70,
or
140
mg/kg
CdCl2
diet
for
90
days.
result
showed
that
striatum
was
damaged
due
a
high
dose
brain,
which
characterized
degeneration
neurons
astrocyte
dysfunction.
Transcriptome
analysis
demonstrated
striatal
astrocytes
transformed
A1
state
under
exposure.
Deeper
investigation
revealed
internalization
gap
junction
protein
connexin
43
responsible
this
transformation.
Eventually,
we
conclude
internalized
anchoring,
process
accompanied
transformation
subtype.
This
study
provides
new
direction
exploring
effects
on
nervous
system
treatment
subsequent
diseases.
Molecular Biomedicine,
Journal Year:
2023,
Volume and Issue:
4(1)
Published: Oct. 16, 2023
Abstract
Ferroptosis,
a
regulated
form
of
cellular
death
characterized
by
the
iron-mediated
accumulation
lipid
peroxides,
provides
novel
avenue
for
delving
into
intersection
metabolism,
oxidative
stress,
and
disease
pathology.
We
have
witnessed
mounting
fascination
with
ferroptosis,
attributed
to
its
pivotal
roles
across
diverse
physiological
pathological
conditions
including
developmental
processes,
metabolic
dynamics,
oncogenic
pathways,
neurodegenerative
cascades,
traumatic
tissue
injuries.
By
unraveling
intricate
underpinnings
molecular
machinery,
contributors,
signaling
conduits,
regulatory
networks
governing
researchers
aim
bridge
gap
between
intricacies
this
unique
mode
multifaceted
implications
health
disease.
In
light
rapidly
advancing
landscape
ferroptosis
research,
we
present
comprehensive
review
aiming
at
extensive
in
origins
progress
human
diseases.
This
concludes
careful
analysis
potential
treatment
approaches
carefully
designed
either
inhibit
or
promote
ferroptosis.
Additionally,
succinctly
summarized
therapeutic
targets
compounds
that
hold
promise
targeting
within
various
facet
underscores
burgeoning
possibilities
manipulating
as
strategy.
summary,
enriched
insights
both
investigators
practitioners,
while
fostering
an
elevated
comprehension
latent
translational
utilities.
revealing
basic
processes
investigating
possibilities,
crucial
resource
scientists
medical
aiding
deep
understanding
effects
situations.
Journal of Agricultural and Food Chemistry,
Journal Year:
2024,
Volume and Issue:
72(13), P. 7411 - 7422
Published: Feb. 23, 2024
Di-(2-ethylhexyl)
phthalate
(DEHP),
as
the
most
common
phthalate,
has
been
extensively
used
a
plasticizer
to
improve
plasticity
of
agricultural
products,
which
pose
severe
harm
human
health.
Mitochondrial
dynamics
and
endoplasmic
reticulum
(ER)
homeostasis
are
indispensable
for
maintaining
mitochondria-associated
ER
membrane
(MAM)
integrity.
In
this
study,
we
aimed
explore
effect
DEHP
on
nervous
system
its
association
with
ER-mitochondria
interaction.
Here,
showed
that
caused
morphological
changes,
motor
deficits,
cognitive
impairments,
blood-brain
barrier
disruption
in
brain.
triggered
stress,
is
mainly
mediated
by
protein
kinase
R-like
(PERK)
signaling.
Moreover,
DEHP-induced
mitofusin-2
(Mfn2)
downregulation
results
imbalance
mitochondrial
dynamics.
Interestingly,
exposure
impaired
MAMs
inhibiting
Mfn2-PERK
Above
all,
study
elucidates
axis-mediated
interaction
phthalate-induced
neurotoxicity
could
be
potentially
developed
novel
therapy
neurological
diseases.
Journal of Agricultural and Food Chemistry,
Journal Year:
2024,
Volume and Issue:
72(27), P. 15334 - 15344
Published: June 25, 2024
Di-2-ethylhexyl
phthalate
(DEHP)
is
frequently
used
as
a
plasticizer
to
enhance
the
plasticity
and
durability
of
agricultural
products,
which
pose
adverse
effects
human
health
environment.
Aquaporin
1
(AQP1)
main
water
transport
channel
protein
involved
in
maintenance
intestinal
integrity.
However,
impact
DEHP
exposure
on
gut
its
potential
mechanisms
remain
elusive.
Here,
we
determined
that
induced
compromised
duodenum
structure,
was
concomitant
with
mitochondrial
structural
injury
epithelial
cells.
Importantly,
caused
inflammatory
cell
damage
strong
response
accompanied
by
activating
TLR4/MyD88/NF-κB
signaling
pathway.
Mechanistically,
directly
inhibits
expression
AQP1
thus
leads
an
response,
ultimately
disrupting
integrity
barrier
function.
Collectively,
our
findings
uncover
role
phthalate-induced
disorders,
could
be
promising
therapeutic
approach
for
treating
patients
disorders
or
diseases.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(2), P. 897 - 897
Published: Jan. 11, 2024
The
hospital
mortality
in
patients
with
ST-segment
elevation
myocardial
infarction
(STEMI)
is
about
6%
and
has
not
decreased
recent
years.
leading
cause
of
death
these
ischemia/reperfusion
(I/R)
cardiac
injury.
It
quite
obvious
that
there
an
urgent
need
to
create
new
drugs
for
the
treatment
STEMI
based
on
knowledge
pathogenesis
I/R
injury,
particular,
molecular
mechanism
ferroptosis.
In
this
study,
it
was
demonstrated
ferroptosis
involved
development
antitumor
drug-induced
cardiomyopathy,
diabetic
septic
inflammation.
There
indirect
evidence
participates
stress-induced
activation
AMPK,
PKC,
ERK1/2,
PI3K,
Akt
prevents
inhibition
HO-1
alleviates
roles
GSK-3β
NOS
regulation
require
further
study.
stimulation
Nrf2,
STAT3
TLR4
NF-κB
promotes
cardiomyocytes.
MiR-450b-5p
miR-210-3p
can
increase
tolerance
cardiomyocytes
hypoxia/reoxygenation
through
Circ_0091761
RNA,
miR-214-3p,
miR-199a-5p,
miR-208a/b,
miR-375-3p,
miR-26b-5p
miR-15a-5p
aggravate
Particle and Fibre Toxicology,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: April 1, 2024
Abstract
Background
Amorphous
silica
nanoparticles
(SiNPs)
have
been
gradually
proven
to
threaten
cardiac
health,
but
pathogenesis
has
not
fully
elucidated.
Ferroptosis
is
a
newly
defined
form
of
programmed
cell
death
that
implicated
in
myocardial
diseases.
Nevertheless,
its
role
the
adverse
effects
SiNPs
described.
Results
We
first
reported
induction
cardiomyocyte
ferroptosis
by
both
vivo
and
vitro
.
The
sub-chronic
exposure
through
intratracheal
instillation
aroused
injury,
characterized
significant
inflammatory
infiltration
collagen
hyperplasia,
accompanied
elevated
CK-MB
cTnT
activities
serum.
Meanwhile,
activation
was
certified
extensive
iron
overload,
declined
FTH1
FTL,
lipid
peroxidation.
correlation
analysis
among
detected
indexes
hinted
responsible
for
SiNPs-aroused
injury.
Further,
tests,
triggered
overload
peroxidation
cardiomyocytes.
Concomitantly,
altered
expressions
TfR,
DMT1,
FTH1,
FTL
indicated
dysregulated
metabolism
cardiomyocytes
upon
SiNP
stimuli.
Also,
shrinking
mitochondria
with
ridge
fracture
ruptured
outer
membrane
were
noticed.
To
note,
inhibitor
Ferrostatin-1
could
effectively
alleviate
SiNPs-induced
peroxidation,
cytotoxicity.
More
importantly,
mechanistic
investigations
revealed
miR-125b-2-3p-targeted
HO-1
as
key
player
SiNPs,
probably
regulating
intracellular
mediate
ensuing
Conclusions
Our
findings
firstly
underscored
fact
mediated
miR-125b-2-3p/HO-1
signaling
contributor
which
be
importance
elucidate
toxicity
provide
new
insights
into
future
safety
applications
SiNPs-related
nano
products.
Graphical
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: Jan. 24, 2025
Abstract
Environmental
pollution
represents
a
significant
public
health
concern,
with
the
potential
risks
associated
environmental
pollutants
receiving
considerable
attention
over
an
extended
period.
In
recent
years,
substantial
body
of
research
has
been
dedicated
to
this
topic.
Since
discovery
ferroptosis,
iron-dependent
programmed
cell
death
typically
characterized
by
lipid
peroxidation,
in
2012,
there
have
advances
study
its
role
and
mechanism
various
diseases.
A
growing
number
studies
also
demonstrated
involvement
ferroptosis
damage
caused
organism
pollutants,
molecular
mechanisms
involved
partially
elucidated.
The
targeting
be
effective
means
ameliorating
PM2.5,
organic
inorganic
ionizing
radiation.
This
review
begins
providing
summary
most
important
ferroptosis.
It
then
proceeds
offer
critical
analysis
effects
induced
pollutants.
Furthermore,
as
is
case
all
rapidly
evolving
areas,
are
numerous
unanswered
questions
challenges
pertaining
pollutant-induced
which
we
discuss
attempt
provide
some
directions
clues
for
future
field.
