BMC Public Health,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: Feb. 21, 2025
Heavy
metals
(e.g.,
cadmium,
lead,
mercury,
etc.)
can
infiltrate
the
human
body
via
diverse
routes,
with
a
propensity
to
accumulate
in
kidney
cortex,
thereby
precipitating
dysfunction.
Vitamin
D
has
been
implicated
mitigating
oxidative
stress
and
inflammatory
reactions
triggered
by
heavy
metal
exposure.
However,
interplay
between
toxicity
vitamin
deficiency
context
of
incipient
injury
remains
an
underexplored
area
research.
Utilizing
data
from
National
Health
Nutrition
Examination
Survey
spanning
2001
2004,
Our
methodology
leveraged
spline
smoothing
within
framework
generalized
additive
models
more
vividly
elucidate
impact
exposure
serum
levels
on
trajectory
early
biomarkers
(including
albumin-to-creatinine
ratio,
β-2
microglobulin
(B2M),
cystatin
C
(CYST),
estimated
glomerular
filtration
rate
(eGFR)
(serum
creatinine(SCr)-based(eGFR),
CYST-based
eGFR,
SCr-CYST-based
eGFR).
Furthermore,
we
conducted
interaction
analysis
assess
combined
effects
injury.
The
cohort
comprised
2,422
adults.
results
indicated
that
cadmium
were
positively
correlated
B2M,
CYST,
negatively
eGFRc,
eGFRs.
Similarly,
lead
showed
positive
correlation
ACR,
negative
eGFRc&s.
In
contrast,
mercury
CYST
eGFRc.
addition,
there
was
indicators
(P
for
interaction:
B2M:
0.028,
CYST:
0.038,
eGFRc&s:
0.011).
This
study
suggests
increased
risk
It
highlights
potential
importance
targeted
supplementation
reduction
these
findings
warrant
validation
through
further
prospective
Journal of Advanced Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Jan. 1, 2024
Arsenic
has
been
ranked
as
the
most
hazardous
substance
by
U.S.
Agency
for
Toxic
Substances
and
Disease
Registry.
Environmental
arsenic
exposure-evoked
health
risks
have
become
a
vital
public
concern
worldwide
owing
to
widespread
existence
of
arsenic.
Multi-omics
is
revolutionary
technique
data
analysis
providing
an
integrated
view
bioinformation
comprehensively
systematically
understanding
elaborate
mechanism
diseases.
This
study
aimed
at
uncovering
potential
contribution
liver-microbiota-gut
axis
in
chronic
inorganic
exposure-triggered
biotoxicity
chickens
based
on
multi-omics
technologies.
Forty
Hy-Line
W-80
laying
hens
were
chronically
exposed
sodium
arsenite
with
dose-dependent
manner
(administered
drinking
water
containing
10,
20,
or
30
mg/L
arsenic,
respectively)
42
d,
followed
transcriptomics,
serum
non-targeted
metabolome,
16S
ribosomal
RNA
gene
sequencing
accordingly.
intervention
induced
serious
chicken
liver
dysfunction,
especially
severe
fibrosis,
simultaneously
altered
ileal
microbiota
populations,
impaired
intestinal
barrier,
further
drove
enterogenous
lipopolysaccharides
translocation
via
portal
vein
circulation
aggravating
damage.
Furtherly,
injured
disturbed
bile
acids
(BAs)
homoeostasis
through
strongly
up-regulating
BAs
synthesis
key
rate-limiting
enzyme
CYP7A1,
inducing
excessive
total
accumulation,
accompanied
massive
primary
BA—chenodeoxycholic
acid.
Moreover,
concentrations
secondary
BAs—ursodeoxycholic
acid
lithocholic
markedly
repressed,
which
might
involve
repressed
dehydroxylation
Ruminococcaceae
Lachnospiraceae
families.
Abnormal
metabolism
turn
promoted
injury,
ultimately
perpetuating
pernicious
circle
chickens.
Notably,
obvious
depletion
abundance
four
profitable
microbiota,
Christensenellaceae,
Ruminococcaceae,
Muribaculaceae,
Faecalibacterium,
correlated
tightly
this
hepato-intestinal
process
Our
demonstrates
that
exposure
evokes
disruption
establishes
scientific
basis
evaluating
risk
environmental
pollutant
Oxidative Medicine and Cellular Longevity,
Journal Year:
2022,
Volume and Issue:
2022, P. 1 - 20
Published: Feb. 1, 2022
Osteoarthritis
(OA)
is
a
chronic
degenerative
disease
featured
by
cartilage
erosion
and
inflammation.
Luteolin,
member
of
the
flavonoid
family,
has
been
shown
to
exert
anti-inflammatory
antioxidative
activities.
However,
potential
biological
effects
underlying
mechanism
luteolin
on
chondrocytes
OA
progression
remain
largely
elusive.
In
this
study,
effect
were
investigated
in
vitro
vivo.
Our
data
revealed
that
inhibited
H2O2-induced
cell
death,
apoptosis,
oxidative
stress,
programmed
necrosis,
inflammatory
mediator
production
primary
murine
chondrocytes.
addition,
could
activate
AMPK
Nrf2
pathways,
serves
as
positive
upstream
regulator
Nrf2.
vivo
results
demonstrated
therapeutic
DMM
mouse
model.
Collectively,
our
findings
showed
might
serve
novel
effective
treatment
for
provided
new
research
direction
clinical
therapies.
RSC Advances,
Journal Year:
2023,
Volume and Issue:
13(28), P. 19429 - 19446
Published: Jan. 1, 2023
Based
on
the
sensing
mechanism,
Hg
2+
ion
materials
developed
in
recent
years
were
systematically
discussed,
classified
into
seven
types,
and
their
corresponding
fluorescence
mechanisms
briefly
introduced.
Ecotoxicology and Environmental Safety,
Journal Year:
2023,
Volume and Issue:
262, P. 115331 - 115331
Published: Aug. 7, 2023
Acetaminophen
(APAP)
overdose
has
long
been
considered
a
major
cause
of
drug-induced
liver
injury.
Ferroptosis
is
type
programmed
cell
death
mediated
by
iron-dependent
lipid
peroxidation.
Endoplasmic
reticulum
(ER)
stress
systemic
response
triggered
the
accumulation
unfolded
or
misfolded
proteins
in
ER.
and
ER
have
proven
to
contribute
progression
APAP-induced
acute
injury
(ALI).
It
was
reported
that
salidroside
protects
against
ALI,
but
potential
mechanism
remain
unknown.
In
this
study,
male
C57BL/6
J
mice
were
intraperitoneally
(i.p.)
injected
APAP
(500
mg/kg)
induce
an
ALI
model.
Salidroside
i.p.
at
dose
100
mg/kg
2
h
prior
administration.
Mice
sacrificed
12
after
injection
serum
obtained
for
histological
biochemistry
analysis.
AML12
cells
used
vitro
assays.
The
results
indicated
mitigated
glutathione
degradation
via
inhibiting
cation
transport
regulator
homolog
1
(CHAC1)
attenuate
ferroptosis,
simultaneously
suppressing
PERK-eIF2α-ATF4
axis-mediated
stress,
thus
alleviating
ALI.
However,
PERK
activator
CCT020312
overexpression
ATF4
inhibited
protective
function
on
CHAC1-mediated
ferroptosis.
Besides
this,
activation
AMPK/SIRT1
signaling
pathway
demonstrated
effect
Interestingly,
selective
inhibition
SIRT1
ameliorated
effects
Overall,
plays
significant
part
mitigation
activating
inhibit
stress-mediated
ferroptosis
ATF4-CHAC1
axis.
Analytical Chemistry,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 6, 2025
Mercury
ions
(Hg2+)
have
been
found
to
disrupt
the
body's
antioxidant
defense
mechanisms,
leading
oxidative
stress
and
physiological
dysfunction.
Early
diagnosis
real-time
monitoring
of
Hg2+
fluctuations
in
organ
damage
are
crucial
but
limited
due
lack
noninvasive
deep
tissue
imaging
probes.
Herein,
a
Hg2+-triggered
targeted
NIR-II
fluorescence/photoacoustic
(PA)
dual-mode
molecular
probe
(NHG-2)
was
developed
for
Hg2+-induced
acute
liver
kidney
injury
mice.
NHG-2
designed
through
rational
adjustment
conjugated
ring
structure
further
screening
processes,
enabling
it
sensitively
recognize
subsequently
open
mitochondrial
targeting,
producing
fluorescence/PA
signals.
This
allowed
injury,
demonstrating
excellent
detection
sensitivity.
Furthermore,
can
be
utilized
evaluate
efficacy
N-acetylcysteine
(NAC)
dual
signal
indication.
Mechanism
studies
suggested
that
NAC
activated
Akt/Nrf2
signaling
pathway,
reversed
changes
related
biomarkers,
restored
membrane
potential.
Thus,
this
study
not
only
presents
first
specific
also
provides
potential
tool
early
treatment
evaluation
pathogenesis
study.