Journal of Zhejiang University (Medical Sciences),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 1, 2024
It
has
been
confirmed
that
exposure
to
various
metal
pollutants
can
induce
neurotoxicity,
which
is
closely
associated
with
the
occurrence
and
development
of
neurological
disorders.
Ferroptosis
a
form
cell
death
in
response
pollutant
it
related
oxidative
stress,
iron
metabolism
lipid
peroxidation.
Recent
studies
have
revealed
ferroptosis
plays
significant
role
neurotoxicity
induced
by
metals
such
as
lead,
cadmium,
manganese,
nickel,
antimony.
Lead
triggers
through
disorder
inflammation.
Cadmium
ion
metabolism,
stress
signaling
pathways
IRE1/JNK/FTH1.
Manganese
promote
mitochondrial
dysfunction,
stress.
Nickel
influencing
function,
disrupting
homeostasis
facilitating
peroxidation
central
nervous
system.
Antimony
glutathione
depletion
activating
autophagy,
resulting
excessive
intracellular
deposition
ultimately
causing
ferroptosis.
This
article
reviews
effects
on
ferroptosis-related
indicators
discusses
specific
mechanisms
each
may
provide
references
identify
targets
preventing
develop
treatment
strategies
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: May 17, 2023
Subarachnoid
hemorrhage
(SAH)
is
a
cerebrovascular
accident
with
an
acute
onset,
severe
disease
characteristics,
and
poor
prognosis.
Within
72
hours
after
the
occurrence
of
SAH,
sequence
pathological
changes
occur
in
body
including
blood-brain
barrier
breakdown,
cerebral
edema,
reduced
flow
that
are
defined
as
early
brain
injury
(EBI),
it
has
been
demonstrated
EBI
exhibits
obvious
correlation
Ferroptosis
novel
programmed
cell
death
mode.
induced
by
iron-dependent
accumulation
lipid
peroxides
reactive
oxygen
species
(ROS).
involves
abnormal
iron
metabolism,
glutathione
depletion,
peroxidation.
Recent
study
revealed
ferroptosis
involved
significantly
correlated
With
gradual
realization
importance
ferroptosis,
increasing
number
studies
have
conducted
to
examine
this
process.
This
review
summarizes
latest
work
field
tracks
current
research
progress.
We
focused
on
reduction
systems
centered
GSH/GPX4
system,
other
newly
discovered
GSH/GPX4-independent
antioxidant
systems,
their
related
targets
context
injury.
Additionally,
we
examined
certain
regulatory
mechanisms
studied
fields
but
not
SAH.
A
link
between
oxidative
stress
described.
highlight
future
direction
provides
new
ideas
for
follow-up
research.
Current Research in Toxicology,
Journal Year:
2024,
Volume and Issue:
6, P. 100170 - 100170
Published: Jan. 1, 2024
The
objective
of
the
present
narrative
review
was
to
synthesize
existing
clinical
and
epidemiological
findings
linking
manganese
(Mn)
exposure
biomarkers
autism
spectrum
disorder
(ASD)
attention
deficit
hyperactivity
(ADHD),
discuss
key
pathophysiological
mechanisms
neurodevelopmental
disorders
that
may
be
affected
by
this
metal.
Existing
data
demonstrated
both
direct
inverse
association
between
Mn
body
burden
ASD,
or
lack
any
relationship.
In
contrast,
majority
studies
revealed
significantly
higher
levels
in
subjects
with
ADHD,
as
well
relationship
inattention
scores
children,
although
several
reported
contradictory
results.
laboratory
impaired
animals
following
associated
dopaminergic
dysfunction
neuroinflammation.
Despite
evidence
on
Mn-induced
neurobiological
alterations
patients
ASD
a
plethora
neurotoxic
effects
overexposure
interfere
pathogenesis
inherent
these
disorders.
Specifically,
overload
shown
impair
not
only
neurotransmission,
but
also
affect
metabolism
glutamine/glutamate,
GABA,
serotonin,
noradrenaline,
thus
affecting
neuronal
signaling.
turn,
its
ability
induce
oxidative
stress,
apoptosis,
neuroinflammation,
and/or
neurogenesis.
Nonetheless,
additional
detailed
are
required
evaluate
environmental
at
wide
range
concentrations
estimate
potential
dose-dependent
effects,
genetic
factors
association.
Animals,
Journal Year:
2024,
Volume and Issue:
14(4), P. 561 - 561
Published: Feb. 7, 2024
Cadmium
(Cd)
pollution
has
become
a
global
issue
due
to
industrial
and
agricultural
developments.
However,
the
molecular
mechanism
of
Cd-induced
detrimental
effects
relevant
signal
transduction/metabolic
networks
are
largely
unknown
in
marine
fishes.
Here,
greenfin
horse-faced
filefish
(Thamnaconus
septentrionalis)
were
exposed
5.0
mg/L
Cd
up
7
days.
We
applied
both
biochemical
methods
multi-omics
techniques
investigate
how
gills
respond
exposure.
Our
findings
revealed
that
exposure
caused
formation
reactive
oxygen
species
(ROS),
which
turn
activated
MAPK
apoptotic
pathways
alleviate
oxidative
stress
cell
damage.
Glycolysis,
protein
degradation,
as
well
fatty
acid
metabolism
might
assist
meet
requirements
nutrition
energy
under
stress.
also
found
long-term
(7
days,
“long-term”
means
compared
12
48
h)
accumulation
succinate,
would
trigger
an
inflammatory
response
start
immunological
process.
Moreover,
ferroptosis
induce
inflammation.
Overall,
stress,
disturbance,
immune
filefish.
conclusions
can
be
used
references
for
safety
risk
assessment
economic
Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
279, P. 116481 - 116481
Published: May 23, 2024
Manganese
(Mn)
overexposure
has
been
associated
with
the
development
of
neurological
damage
reminiscent
Parkinson's
disease,
while
underlying
mechanisms
have
yet
to
be
fully
characterized.
This
study
aimed
investigate
leading
injury
in
dopaminergic
neurons
induced
by
Mn
and
identify
novel
treatment
approaches.
In
vivo
vitro
models,
ICR
mice
neuron-like
PC12
cells
were
exposed
Mn,
respectively.
We
treated
them
anti-ferroptotic
agents
ferrostatin-1
(Fer-1),
deferoxamine
(DFO),
HIF-1α
activator
dimethyloxalylglycine
(DMOG)
inhibitor
LW6.
also
used
p53-siRNA
verify
mechanism
Mn-induced
neurotoxicity.
Fe
concentrations
increased
brains
overexposed
Mn.
Additionally,
Mn-exposed
exhibited
movement
impairment
encephalic
pathological
changes,
decreased
HIF-1α,
SLC7A11,
GPX4
proteins
p53
protein
levels.
Fer-1
protective
effects
against
both
behavioral
biochemical
changes.
Consistently,
vitro,
exposure
caused
ferroptosis-related
changes
levels,
all
ameliorated
Fer-1.
Upregulation
DMOG
alleviated
Mn-associated
ferroptosis,
LW6
exacerbated
neurotoxicity
through
downregulating
HIF-1α.
knock-down
rescued
ferroptosis
without
altering
expression.
resulted
neurons,
mediated
HIF-1α/p53/SLC7A11
pathway.
