Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
278, P. 116424 - 116424
Published: May 8, 2024
Epidemiological
studies
have
reported
associations
between
heavy
metals
and
renal
function.
However,
longitudinal
are
required
to
further
validate
these
explore
the
interactive
effects
of
on
function
their
directional
influence.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(23), P. 16558 - 16558
Published: Nov. 21, 2023
Cadmium
is
a
heavy
metal
that
increasingly
contaminates
food
and
drink
products.
Once
ingested,
cadmium
exerts
toxic
effects
pose
significant
threat
to
human
health.
The
nervous
system
particularly
vulnerable
prolonged,
low-dose
exposure.
This
review
article
provides
an
overview
of
cadmium’s
primary
mechanisms
neurotoxicity.
gains
entry
into
the
via
zinc
calcium
transporters,
altering
homeostasis
for
these
ions.
within
system,
disrupts
mitochondrial
respiration
by
decreasing
ATP
synthesis
increasing
production
reactive
oxygen
species.
also
impairs
normal
neurotransmission
neurotransmitter
release
asynchronicity
disrupting
signaling
proteins.
furthermore
blood–brain
barrier
alters
regulation
glycogen
metabolism.
Together,
represent
multiple
sites
biochemical
perturbation
result
in
cumulative
damage
which
can
increase
risk
neurological
neurodegenerative
disorders.
Understanding
way
its
critical
developing
effective
treatment
prevention
strategies
against
cadmium-induced
neurotoxic
insult.
Toxics,
Journal Year:
2024,
Volume and Issue:
12(6), P. 388 - 388
Published: May 26, 2024
Cadmium
(Cd),
a
prevalent
environmental
contaminant,
exerts
widespread
toxic
effects
on
human
health
through
various
biochemical
and
molecular
mechanisms.
This
review
encapsulates
the
primary
pathways
which
Cd
inflicts
damage,
including
oxidative
stress
induction,
disruption
of
Ca2+
signaling,
interference
with
cellular
signaling
pathways,
epigenetic
modifications.
By
detailing
absorption,
distribution,
metabolism,
excretion
(ADME)
Cd,
alongside
its
interactions
components
such
as
mitochondria
DNA,
this
paper
highlights
extensive
damage
caused
by
Cd2+
at
tissue
levels.
The
role
in
inducing
stress—a
pivotal
mechanism
behind
toxicity—is
discussed
emphasis
how
it
disrupts
balance
between
oxidants
antioxidants,
leading
to
apoptosis.
Additionally,
covers
Cd’s
impact
like
Mitogen-Activated
Protein
Kinase
(MAPK),
Nuclear
Factor
kappa-light-chain-enhancer
activated
B
cells
(NF-κB),
Tumor
53
(p53)
illustrating
these
contributes
pathological
conditions
carcinogenesis.
DNA
methylation
histone
modifications,
are
also
explored
explain
long-term
gene
expression
disease
manifestation.
comprehensive
analysis
not
only
elucidates
mechanisms
toxicity
but
underscores
critical
need
for
enhanced
strategies
mitigate
public
implications.
Atmosphere,
Journal Year:
2025,
Volume and Issue:
16(2), P. 225 - 225
Published: Feb. 17, 2025
Cadmium
(Cd)
is
a
pervasive
environmental
and
industrial
toxin
that
poses
significant
health
risks.
It
readily
moves
through
soil–plant
systems,
leading
to
global
contamination
human
exposure
diet,
smoking,
pollution.
The
main
purpose
of
this
review
explore
the
effect
Cd
on
physiological
processes
different
bodies’
organs,
including
bones,
kidneys,
liver,
as
well
immune,
cerebrovascular,
cardiovascular,
reproductive
systems.
Accumulation
in
body
can
result
poisoning
with
severe
impacts
bone
kidney
health,
reduced
mineral
density
due
renal
damage.
Research
has
linked
lung
cancer
pulmonary
toxicity,
elevated
urinary
biomarkers
suggest
compromised
function.
also
affects
immune
systems;
liver;
contributing
various
diseases
by
disrupting
blood
pressure
calcium
regulation,
causing
oxidative
stress
DNA
damage,
impairing
cell
functions.
Ongoing
research
essential
fully
understand
Cd-induced
toxicological
effects
develop
effective
interventions
prevent
mitigate
Microorganisms,
Journal Year:
2025,
Volume and Issue:
13(3), P. 470 - 470
Published: Feb. 20, 2025
Schizophyllum
commune
is
an
edible
fungus
with
high
medicinal
value,
but
exposure
to
heavy-metal
pollution
poses
significant
health
risks.
Cadmium
(Cd)
toxicity
inhibits
fungal
growth
and
leads
Cd
accumulation
in
the
mycelium.
However,
regulatory
mechanisms
of
Cd-induced
inhibition
remain
poorly
understood.
Here,
S.
20R-7-F01
was
cultured
Cd-supplemented
minimal
medium
(MM)
investigate
response
exposure.
We
found
that
resulted
a
Cd-dependent
increase
endogenous
nitric
oxide
(NO)
levels.
NO
production
primarily
mediated
by
nitrate
reductase
(NR)
pathway.
alleviated
inhibiting
NR
activity
or
scavenging
NO,
highlighting
role
stress
responses.
Furthermore,
enhance
chitinase
activity,
thereby
promoting
cell
wall
leading
inhibition.
These
results
reveal
novel
mechanism
which
copes
stress.
This
study
highlights
potential
manipulating
levels
as
strategy
tolerance
pollution,
providing
new
avenue
for
managing
environmental
stresses
fungi
protecting
human
health.
Cadmium
(Cd)
is
a
hazardous
unnecessary
transition
metal
that
harmful
to
people
and
animals.
naturally
prevalent
in
the
environment
frequently
obtained
from
agriculture
industrial
processes.
Humans
are
typically
exposed
Cd
through
filthy
food
water,
inhalation,
cigarette
smoking.
stored
plants
animals
has
lengthy
half-life
of
25–30
years.
Observational
l
evidence
suggests
occupational
environmental
exposure
may
be
connected
malignancies
breast,
lung,
prostate,
nasopharynx,
pancreas,
kidney,
as
well
an
increased
risk
osteoporosis.
Because
their
capacity
generate
metallothioneins
(MT),
which
Cd-inducible
proteins
protect
cells,
liver
kidneys
particularly
sensitive
effects
Cd.
Cadmium-induced
oxidative
stress
likely
contribute
variety
kidney
illnesses,
mitochondrial
damage
possible
mechanism,
these
organelles
play
important
role
generation
reactive
oxygen
species
(ROS)
intracellular
targets
for
The
determination
dietary
consumption
critical
step
estimating
body
burden
associated
health
consequences.
Chronic
known
have
substantial
influence
on
kidneys,
most
vulnerable
toxicity.
Urinary
(UC),
proportional
relationship
between
accumulation
excretion
via
urine,
reliable
indicator
exposure.
This
chapter
outlines
numerous
pathways
exposure,
impact
human
health,
use
several
biomarkers
measure
This
chapter
delves
into
the
combined
molecular
toxicity
mechanisms
of
heavy
metal
mixtures,
focusing
on
their
pervasive
presence
due
to
industrial
activities
and
impact
human
health.
The
authors
highlight
significance
bioaccumulation
metals
through
ingestion
inhalation,
which
can
lead
various
health
implications.
highlights
multifaceted
effects
mixtures
cardiovascular
system,
contributing
diseases
like
atherosclerosis
hypertension
oxidative
stress
vascular
inflammation.
It
details
interactions
these
with
proteins,
particularly
inhibition
ATPases
promotion
damage,
leading
dysfunction.
briefly
touches
upon
link
between
cadmium
exposure
prostate
cancer,
emphasizing
need
for
further
investigation
underlying
this
association.
Additionally,
it
mentions
potential
zinc
sulfate
olfactory
neuron
subtypes
in
adult
fish,
suggesting
that
disrupt
sensory
systems
aquatic
organisms.
Moreover,
explores
neurotoxicity
metals,
discussing
nervous
system
neurodevelopmental
disorders.
also
examines
male
female
reproductive
systems,
evidence
disruptions
hormone
levels,
sperm
quality,
fertility.
call
enhanced
monitoring
levels
general
population
better
understand
its
They
emphasize
research
by
contribute
health,
inform
clinical
treatments
public
interventions.
By
highlighting
bioaccumulation,
stress,
time-dependent
responses,
study
sheds
light
urgent
intervention
strategies
mitigate
adverse
environment.