Journal of Food Science,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 22, 2024
Abstract
To
investigate
the
effect
of
bound
phenolics
extracts
(BPEs)
jujube
peel
on
relieving
cadmium
(Cd)‐induced
toxicity
and
its
mechanism,
behavioral
deficits,
lipid
accumulation,
fatty
acid
synthesis‐related
gene
expression
in
Caenorhabditis
elegans
Cd
exposure
group
BPEs
improvement
groups
were
determined
compared.
The
results
showed
that
significantly
improved
Cd‐induced
deficits
C.
,
no
significant
differences
could
be
found
low‐dose
(12.5
µg/mL)
high‐dose
(100
groups.
treatment
effectively
intestinal
injury
lipofuscin
accumulation.
Especially,
oil
red
O
staining
intensity
treated
with
at
50
µg/mL
was
reduced
by
12.60%.
controlled
increase
content
C16:0,
C16:1,
C18:0,
C18:1,
C18:2
induced
regulating
accumulation
Escherichia
coli
OP50
.
upregulating
oleic
E.
Furthermore,
downregulated
This
research
reveal
mechanism
provide
a
theoretical
basis
for
development
functional
foods
rich
polyphenols.
Practical
Application
Jujube
peel,
by‐product
processing,
is
usually
discarded
due
to
coarse
texture.
However,
has
been
proven
possess
abundant
polyphenols,
polysaccharides,
cyclic
adenosine
phosphate.
In
addition,
our
previous
research,
perform
better
lowering
than
free
extracts.
study
further
base
research.
It
realize
comprehensive
utilization
by‐products
processing.
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
Advanced Science,
Journal Year:
2024,
Volume and Issue:
11(30)
Published: June 5, 2024
Cadmium
(Cd)
is
a
neurotoxic
contaminant
that
induces
cognitive
decline
similar
to
observed
in
Alzheimer's
disease
(AD).
Autophagic
flux
dysfunction
attributed
the
pathogenesis
of
AD,
and
this
study
aimed
investigate
effect
autophagy
on
environmental
Cd-induced
AD
progression
underlying
mechanism.
Here,
Cd
exposure
inhibited
autophagosome-lysosome
fusion
impaired
lysosomal
function,
leading
defects
autophagic
clearance
then
APP
accumulation
nerve
cell
death.
Proteomic
analysis
coupled
with
Ingenuity
Pathway
Analysis
(IPA)
identified
SIRT5
as
an
essential
molecular
target
Cd-impaired
flux.
Mechanistically,
hampered
expression
SIRT5,
thus
increasing
succinylation
RAB7A
at
lysine
31
inhibiting
activity,
which
contributed
blockade.
Importantly,
overexpression
led
restoration
blockade,
alleviation
Aβ
deposition
memory
deficits,
desuccinylation
Cd-exposed
FAD
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
15
Published: Jan. 6, 2025
Cadmium
(Cd)
and
polystyrene
microplastics
(PS-MPs),
two
ubiquitous
environmental
contaminants,
produce
unique
synergistic
toxicity
when
co-existing.
Key
unanswered
questions
include
specific
effects
on
liver
function
potential
mechanisms.
In
this
study,
C57BL/6
mice
AML12
cells
were
used
to
establish
in
vivo
vitro
models
elucidate
the
of
combined
exposure
PS-MPs
Cd
their
The
results
showed
that
caused
significantly
more
damage
than
alone.
As
observed
by
transmission
electron
microscopy
(TEM),
number
autophagosomes
was
increased
co-treated
group.
addition,
autophagic
flux
assayed
RFP-GFP-LC3,
a
reporter
system
expressing
dual
fluorescent
proteins,
which
an
overwhelming
enhancement
co-exposure
compared
To
further
investigate
involvement
carnitine
palmitoyltransferase1(CPT1)
injury
induced
PS-MPs,
we
co-exposed
Baicalin,
activator
CPT1,
with
Cd,
activation
CPT1
alleviated
impairment
fluxes
changes
lipid
accumulation
associated
protein
levels.
conclusion,
concurrent
resulted
blockage
hepatic
pathway
aggravated
toxic
liver.
Activation
could
alleviate
Cd-induced
autophagy
thus
reducing
injury.
Poultry Science,
Journal Year:
2024,
Volume and Issue:
103(7), P. 103817 - 103817
Published: May 1, 2024
Cadmium
(Cd)
is
a
common
environmental
pollutant
associated
with
an
increased
incidence
of
renal
metabolic
diseases.
Luteolin
(Lut),
natural
flavonoid,
widely
used
for
its
multifaceted
therapeutic
properties
in
inflammatory
However,
whether
Lut
protects
against
Cd-induced
nephrotoxicity
still
equivocal.
The
present
study
investigated
the
effects
supplementation
on
oxidative
stress,
inflammation
and
metabolism
their
related
mechanisms.
Therefore,
40
chickens
were
treated
Cd
and/or
automatic
water
free
food
intake
1
mo
then
kidney
tissues
collected
to
explore
this
issue.
In
study,
exposure
induced
glycolipid
disorders
resultant
damage
by
periodic
acid
Schiff
(PAS)
staining,
Oil
Red
O
total
cholesterol
(TC),
triglyceride
(TG),
glucose
(Glu)
levels
kidney,
which
significantly
ameliorated
Lut.
Moreover,
also
normalized
expression
factors
Cd-disturbed
metabolism,
improving
homeostasis,
contributing
alleviating
damage.
Furthermore,
demonstrated
potential
stress
enhancing
antioxidant
capacity
inhibiting
cytokine
production
tissues.
Mechanistically,
activated
AMPK/SIRT1/FOXO1
signaling
pathway,
attenuating
responses,
ameliorating
disturbance.
conclusion,
these
observations
demonstrate
that
treatment
activates
decreases
response,
may
contribute
prevent
disorder
consequent
Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
278, P. 116405 - 116405
Published: May 1, 2024
Cadmium
(Cd)
exposure
is
considered
as
non-infectious
stressor
to
human
and
animal
health.
Recent
studies
suggest
that
the
immunotoxicity
of
low
dose
Cd
not
directly
apparent,
but
disrupts
immune
responses
when
infected
with
some
bacteria
or
virus.
But
how
alters
adaptive
immunity
organ
cells
remains
unclear.
In
this
study,
we
applied
lipopolysaccharide
(LPS,
infectious
stressor)
induced
inflammation
in
spleen
tissues
T
cells,
investigated
effects
after
underlying
mechanism.
promoted
LPS-induced
expressions
inflammatory
factors,
abnormal
initiation
autophagy,
blocked
autophagic
flux.
The
under
LPS
activation
were
reversed
by
autophagy
promoter
Rapamycin.
Under
conditions,
also
oxidative
stress
increasing
levels
reactive
oxygen
species
(ROS)
malondialdehyde
(MDA),
reducing
total
antioxidant
capacity
(T-AOC)
activity.
increased
superoxide
dismutase
(SOD)
activity
might
be
a
negative
feedback
passive
regulation
stress.
Cd-increased
flux
inhibition
TNF-α
expression
ROS
scavenger
α-tocopherol
(TCP).
Furthermore,
condition,
toll-like
receptor
4
(TLR4)/IκBα/NFκ-B
signaling
pathway
TLR4
protein
stability,
which
abolished
pretreatment
present
study
confirmed
that,
ROS-mediated
inhibiting
degradation
TLR4,
cells.
This
identified
mechanism
Cd-aggravated
stress,
could
arouse
public
attention
synergistic
toxicity
bacterial
virus
infection.