Background
Diabetic
cataract
(DC)
is
a
major
cause
of
blindness,
with
its
pathogenesis
involving
oxidative
stress
and
ferroptosis,
according
to
recent
studies.
Poultry Science,
Год журнала:
2024,
Номер
103(9), С. 104011 - 104011
Опубликована: Июнь 22, 2024
Exposure
to
copper
(Cu)
has
been
associated
with
metabolic
disorders
in
animals
and
humans,
but
the
underlying
mechanism
remains
unclear.
One-day-old
broiler
chickens,
numbering
a
total
of
192,
were
nourished
dietary
intakes
that
contained
varying
concentrations
Cu,
specifically
11,
110,
220,
330
mg/kg
for
period
extending
over
duration
7
wk.
As
result
study,
Cu
exposure
resulted
vacuolization,
fragmentation
mitochondria
cristae,
increase
autophagosomes
hepatocytes.
Metabolomics
analysis
illustrated
caused
59
different
metabolites
liver,
predominantly
glycerophospholipid
pathway,
leading
disruption.
Moreover,
high-Cu
diet
markedly
reduced
levels
AMPKα1,
p-AMPKα1,
mTOR,
p-mTOR
enhanced
expression
autophagy-related
factors
(Atg5,
Dynein,
Beclin1,
LC3-II).
Overall,
chicken
liver
injury
disturbed
processes
mediated
autophagy
primarily
through
AMPK-mTOR
axis.
Metabolites,
Год журнала:
2024,
Номер
14(1), С. 71 - 71
Опубликована: Янв. 22, 2024
Ecological
theories
suggest
that
environmental
factors
significantly
influence
obesity
risk
and
related
syndemic
morbidities,
including
metabolically
abnormal
associated
with
nonalcoholic
fatty
liver
disease
(MASLD).
These
encompass
anthropogenic
influences
endocrine-disrupting
chemicals
(EDCs),
synergistically
interacting
to
induce
metabolic
discrepancies,
notably
in
early
life,
disrupt
processes
adulthood.
This
review
focuses
on
endocrine
disruptors
affecting
a
child’s
MASLD
risk,
independent
of
their
role
as
obesogens
thus
regardless
impact
adipogenesis.
The
plays
pivotal
detoxification
processes,
where
various
lipophilic
molecules
accumulate
parenchyma,
exacerbating
inflammation
functioning
new
anthropogenics
perpetuate
chronic
low-grade
inflammation,
especially
insulin
resistance,
crucial
the
pathogenesis
MASLD.
Archives of Public Health,
Год журнала:
2024,
Номер
82(1)
Опубликована: Март 27, 2024
Abstract
Heavy
metals’
presence
as
environmental
pollutants
has
a
close
link
to
adverse
health
effects.
Frailty,
clinical
syndrome
hallmarked
by
elevated
vulnerability
stressors,
presents
substantial
challenge
in
healthcare.
However,
the
association
between
exposure
heavy
metals
and
frailty
largely
remains
unexplored.
Utilizing
data
from
National
Health
Nutrition
Examination
Survey
(NHANES)
spanning
2003–2018
correlated
with
U.S.
Death
Index
(NDI)
2019,
we
investigated
mortality
outcomes.
Logistic
regression,
Cox
Kaplan-Meier
survival
curves,
weighted
quantile-sum
(WQS)
Bayesian
kernel
machine
regression
(BKMR)
were
employed
assess
metal
incidence
frail
population.
Eight
measured
urine
using
inductively
coupled
plasma
mass
spectrometry
values
adjusted
for
urinary
creatinine,
which
was
used
reflect
exposure.
The
cohort
incorporated
5370
female
participants
aged
45
above,
1518
diagnosed
frailty.
findings
indicated
correlation
specific
metals,
namely
tungsten
(odds
ratio
[OR]:
1.94,
95%
confidence
interval
[CI]:
1.31–2.89),
cobalt
(OR:
1.64,
CI:
1.40–1.93),
cadmium
1.93,
1.52–2.43),
uranium
7.36,
1.53–35.28),
an
risk
of
WQS
BKMR
models
identified
cadmium,
cobalt,
main
contributors
analysis,
after
adjustment
covariates,
suggested
that
higher
levels
lead,
death
patients,
associated
hazard
ratios
(HR)
1.96
(1.53,
2.52)
1.30
(1.13,
1.49),
respectively.
Our
study
revealed
significant
positive
mixtures
onset
middle-aged
older
adults,
along
increased
patients.
Cobalt,
emerged
prominent
frailty,
directly
impacting
long-term
life
expectancy
Pharmacological Research,
Год журнала:
2024,
Номер
205, С. 107251 - 107251
Опубликована: Июнь 12, 2024
Nonalcoholic
fatty
liver
disease
(NAFLD)
is
one
of
the
leading
causes
chronic
worldwide.
Epidemiological
studies
have
reported
that
exposure
population
to
environmental
endocrine-disrupting
chemicals
(EDCs)
associated
with
NAFLD.
However,
EDCs
are
different
types,
and
there
inconsistencies
in
relevant
evidence
descriptions,
which
not
been
systematically
summarized
so
far.
Therefore,
this
study
aimed
determine
association
between
Three
databases,
including
PubMed,
Web
science,
Embase
were
searched,
27
articles
included
study.
Methodological
quality,
heterogeneity,
publication
bias
assessed
using
Newcastle-Ottawa
scale,
I
Environmental Science & Technology,
Год журнала:
2025,
Номер
59(1), С. 268 - 278
Опубликована: Янв. 2, 2025
Arsenic
(As)
is
a
toxic
metalloid
widespread
in
the
environment,
and
its
exposure
has
been
associated
with
variety
of
adverse
health
outcomes.
As
demonstrated
to
cause
nonalcoholic
fatty
liver
disease
(NAFLD),
underlying
epigenetic
mechanisms
remain
largely
unknown.
This
study
aimed
investigate
roles
histone
modifications
low-level
exposure-induced
NAFLD
rats.
The
results
showed
that
caused
lipid
accumulation
upregulated
expression
metabolism-related
genes
Fabp1,
Srebf1,
Apoc3,
while
downregulated
Acox1
Cpt1a
rat
liver.
In
addition,
it
was
found
inorganic
arsenite
(iAsIII)
methylated
DMA,
S-adenosylmethionine
(SAM)
level
decreased,
which
would
contribute
repression
H3K9me1/2
after
exposure.
vitro
studies
revealed
SAM
supplementation
attenuated
by
restoring
HepG2
cells,
further
confirmed
our
animal
results.
Therefore,
suggested
methylation
depleted
SAM,
inhibited
activated
Apoc3
expressions,
leading
upon
Overall,
these
data
shed
new
light
on
role
SAM-mediated
As-triggered
NAFLD,
could
be
useful
for
prevention
intervention
hepatotoxicity
induced
environmental
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 30, 2025
Abstract
Liver
disease
poses
a
significant
threat
to
global
public
health,
with
arsenic
(As)
recognized
as
major
environmental
toxin
contributing
liver
injury.
However,
the
specific
mechanisms
and
protective
effects
of
α‐lipoic
acid
(LA)
remain
unclear.
Therefore,
this
study
employs
network
toxicology
pharmacology
comprehensively
analyze
hepatotoxic
mechanism
As
hepatoprotective
LA,
further
verifies
peroxisomal
β‐oxidation
lipophagy
in
process.
The
analysis
results
show
that
induces
damage
mainly
through
autophagy,
apoptosis,
lipid
metabolism,
oxidative
stress,
whereas
LA
exerts
its
properties
by
regulating
metabolism.
Further
verifications
find
inhibits
SIRT1
expression,
activates
P53
Notch
pathways,
damages
mitochondria,
β‐oxidation,
increases
accumulation,
enhances
liver,
while
intervention
alleviates
As‐induced
accumulation
targeting
SIRT1,
ameliorating
mitochondrial
damage,
enhancing
thereby
alleviating
damage.
This
clarifies
hepatotoxicity
provides
theoretical
basis
for
potential
agent.