Ecotoxicology and Environmental Safety,
Journal Year:
2023,
Volume and Issue:
267, P. 115625 - 115625
Published: Oct. 27, 2023
We
investigated
the
toxicological
mechanism
by
which
perfluorooctane
sulfonate
(PFOS)
induces
liver
injury
via
ferroptosis.
Primary
mouse
hepatocytes
were
treated
with
LD50
=
55
M
PFOS.
Their
cytotoxicity
was
detected
CCK-8
and
LDH
assays,
while
JC-1
staining
used
to
identify
their
mitochondrial
membrane
potential.
GSH-Px,
MDA,
SOD
levels
determined
using
kits,
Fe2
+
FerroOrange
probe
iron
ion
assay
kit.
The
DCFH-DA
examine
ROS
levels,
Western
blot
protein
expressions.
After
treatment
ferroptosis
inhibitor
YL939
BABTA,
ability
of
PFOS
induce
observed.
In
animal
experiments,
we
examined
function
degree
hepatic
mice
as
well
histopathological
changes.
could
hepatocyte
ferroptosis,
BABTA
inhibit
PFOS-induced
increase
in
tissue,
injury.
can
cause
mice,
is
its
mechanism.
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 29, 2024
Abstract
Maternal
health,
specifically
changes
in
the
gut
microbiota,
profoundly
affects
health
of
offspring.
However,
our
understanding
how
microbiota
alterations
during
preconception
period
influence
their
offspring
remains
limited.
In
this
study,
we
are
dedicated
to
investigate
impact
maternal
disturbance
on
enteric
nervous
system
(ENS)
development
mice
and
explore
underlying
mechanisms.
Through
in
vivo
vitro
experiments,
made
a
novel
discovery
that
exposure
antibiotics
before
pregnant
leads
abnormal
offspring’s
ENS,
increasing
susceptibility
water
avoidance
stress.
Supported
by
metagenomic,
targeted
metabolome,
transcriptome
analysis,
identified
antibiotic
disrupts
expression
genes
crucial
for
embryonic
ENS
altering
composition
microbiota.
Furthermore,
multi-omics
analysis
combined
with
Limosilactobacillus
reuteri
(L.
reuteri)
gestational
supplementation
illustrated
metabolites
via
propionate-GPR41-GDNF/RET/SOX10
signaling
pathway.
Our
findings
highlight
critical
importance
maintaining
healthy
proper
Environment & Health,
Journal Year:
2023,
Volume and Issue:
2(2), P. 85 - 94
Published: Dec. 18, 2023
Perfluorooctanoic
acid
(PFOA)
and
perfluorooctanesulfonate
(PFOS)
continue
to
be
extensively
present
in
the
natural
environment
seriously
threaten
human
health.
The
intestinal
tract
is
primary
organ
of
PFOA/PFOS
exposure
due
consumption
contaminated
food
drinking
water.
However,
it
remains
unclear
how
affects
function
overall
aim
this
study
was
investigate
influence
on
absorption
fatty
acids
intestine
underlying
mechanisms
using
three-dimensional
(3D)
organoids.
Our
results
showed
that
PFOS,
but
not
PFOA,
could
significantly
enhance
uptake
capacity
without
obvious
damage
Furthermore,
PFOS
markedly
reduced
protein
levels
ChgA
enteroendocrine
cells,
with
no
observed
impact
aldolase
B+
enterocytes.
Mechanistically,
induced
activation
peroxisome
proliferator-activated
receptor
(PPAR)
α
pathway
organoids,
enhanced
expression
PPARα
target
genes
associated
metabolism,
such
as
Fabp1
Cd36
(fatty
transporter
genes),
Acox1
Pdk4
oxidation
Plin2
Plin3
(lipid
droplet
synthesis
genes).
These
data
suggest
have
potential
affect
epithelium
through
pathway,
its
effect
much
stronger
than
PFOA.
findings
also
highlight
organoids
can
used
a
valuable
model
for
conducting
toxicological
research
environmental
chemicals.
Journal of Environmental Science and Public Health,
Journal Year:
2023,
Volume and Issue:
07(02)
Published: Jan. 1, 2023
Empirical
evidence
from
human
studies
has
demonstrated
a
correlative
relationship
between
perfluorooctane
sulfonate
(PFOS)
exposure
and
increased
risks
of
preeclampsia
fetal
developmental
complications.
Although
experimental
circumstantial
data
suggest
that
PFOS
induces
endothelial
dysfunction,
leading
to
decreased
uterine
arterial
blood
flow
gestational
hypertension,
the
precise
regulatory
mechanisms
responsible
for
this
effect
remain
unknown.
To
address
issue,
we
treated
artery
cells
(hUAECs)
isolated
pregnant
women
with
10
μmol/L
or
vehicle
conducted
comparative
transcriptomic
analyses.
We
identified
total
19
differentially
expressed
genes,
9
which
were
upregulated
down-regulated
in
PFOS-treated
hUAECs.
Pre-ranked
gene
set
enrichment
analysis
unveiled
distinct
activated
genes
involved
osmotic
stress,
cellular
stress
response,
translation
regulation,
metabolic
oxidation-reduction
processes
Furthermore,
treatment
resulted
downregulation
implicated
cardiac
muscle
cell
proliferation,
embryonic
morphogenesis,
proliferation.
In
addition,
observed
differential
splicing
events
2678
hUAECs
exposed
PFOS,
cross-comparison
revealing
4
both
alternatively
spliced
oxidative
development.
conclusion,
study
provides
comprehensive
understanding
molecular
underlying
PFOS-induced
dysfunction
during
pregnancy,
offering
valuable
resource
future
research
field.
