Toxics,
Journal Year:
2024,
Volume and Issue:
12(10), P. 723 - 723
Published: Oct. 4, 2024
Toxicity
mechanisms
of
per-
and
polyfluoroalkyl
substances
(PFASs),
a
chemical
class
present
in
diverse
ecosystems,
as
well
many
their
precursors,
have
been
increasingly
characterized
aquatic
species.
Perfluorooctanesulfonamide
(PFOSA,
C8H2F17NO2S)
is
common
precursor
perfluorooctane
sulfonic
acid
(PFOS),
long-chain
PFAS.
Here,
we
assessed
sub-lethal
endpoints
related
to
development,
oxidative
stress,
transcript
levels,
distance
moved
zebrafish
embryos
larvae
following
continuous
exposure
PFOSA
beginning
at
6
h
post-fertilization
(hpf).
decreased
survival
fish
treated
with
1
µg/L
PFOSA;
however,
the
effect
was
modest
relative
controls
(difference
10%).
Exposure
up
10
did
not
affect
hatch
rate,
nor
it
induce
ROS
7-day-old
fish.
The
activity
larval
100
reduced
solvent
control.
Transcripts
stress
response
apoptosis
were
measured
BCL2-associated
X,
regulator
(bax),
cytochrome
c,
somatic
(cycs),
catalase
(cat),
superoxide
dismutase
2
(sod2)
induced
high
concentrations
PFOSA.
Genes
neurotoxicity
also
levels
acetylcholinesterase
(ache),
elav-like
RNA
binding
protein
3
(elavl3),
growth-associated
43
(gap43),
synapsin
II
(syn2a),
tubulin
(tubb3)
all
increased
higher
exposure.
These
data
improve
our
understanding
potential
toxicity
Environment & Health,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 11, 2025
Perfluorooctanesulfonate
(PFOS),
an
emerging
contaminant
with
widespread
concern,
has
been
associated
the
pathogenesis
of
atherosclerosis
(AS).
As
a
substitute
for
PFOS,
sodium
p-perfluorous
nonenoxybenzenesulfonate
(OBS)
is
extensively
utilized
in
various
applications
and
detected
human
blood.
However,
its
potential
health
risk
AS
remain
unclear.
In
this
study,
we
investigated
comparative
impacts
PFOS
OBS
on
endothelial
dysfunction
atherogenesis.
vivo
Apolipoprotein
E
knockout
(ApoE–/–)
mice
were
exposed
to
0.4
or
4
mg/L
PFOS/OBS
12
weeks.
We
found
that
dyslipidemia
developed
more
rapidly
OBS-exposed
than
PFOS-exposed
mice.
exhibited
higher
enrichment
capacity
both
blood
aortic
tissues
OBS.
Remarkably,
induced
pronounced
inflammatory
response
caused
significant
disruption
barrier
aorta
ApoE–/–
compared
PFOS.
vitro
experiments
showed
OBS,
at
same
exposure
concentrations
durations
as
(0.1–20
μmol/L,
48
h),
effectively
inhibited
cell
viability
umbilical
vein
cells
(HUVECs),
levels
lactate
dehydrogenase
(LDH)
release,
enhanced
adhesion
between
HUVECs
monocytes.
Both
activate
NF-κB
signaling
pathway
upregulate
expression
factors.
Notably,
use
but
not
was
shown
disrupt
junctions
increase
permeability
by
activating
MAPK/ERK
pathway.
Our
findings
suggest
may
lead
have
greater
impact
presenting
risks
cardiovascular
diseases.
Animals,
Journal Year:
2025,
Volume and Issue:
15(4), P. 610 - 610
Published: Feb. 19, 2025
Perfluorooctane
sulfonate
(PFOS)
contamination
poses
a
significant
environmental
threat
due
to
its
widespread
distribution
and
persistence.
However,
the
hepatotoxic
effects
of
PFOS
on
key
aquatic
species,
such
as
crucian
carp,
remain
understudied.
This
study
systematically
investigated
hepatotoxicity
underlying
molecular
mechanisms
associated
with
exposure
in
carp
over
21
day
period.
We
determined
96
h
50%
lethal
concentration
(LC50)
23.17
mg/L.
Histopathological
transcriptomic
analyses
confirmed
PFOS-induced
liver
damage
characterized
by
venous
congestion,
nucleolar
dissolution
cellular
vacuolation.
Transcriptomic
profiling
further
identified
1036
differentially
expressed
genes
(DEGs),
involving
critical
pathways
related
lipid
energy
metabolism,
immunity,
endocrine
regulation.
These
are
integral
development
nonalcoholic
fatty
disease
(NAFLD).
Specifically,
DEGs
metabolism
showed
changes,
while
those
involved
indicated
disrupted
ATP
production
mitochondrial
function.
Genes
immune
response
revealed
an
upregulation
pro-inflammatory
markers,
hormone
regulation
highlighted
alterations
signaling.
Our
findings
emphasized
that
exhibits
acute
toxicity
potentially
inducing
disrupting
multiple
physiological
systems.
research
provides
theoretical
foundation
for
mitigating
pollution
protecting
eco-health,
contributing
broader
ecological
conservation
biology
discussions.
Toxics,
Journal Year:
2025,
Volume and Issue:
13(4), P. 269 - 269
Published: April 1, 2025
Perfluoroctane
sulfonate
(PFOS)
is
an
emerging
pollutant
widely
existing
in
aquatic
environments
that
has
attracted
many
scholars’
attention.
Cherax
quadricarinatus
(C.
quadricarinatus)
are
crustaceans
live
freshwater
environments.
This
study
aimed
to
investigate
the
long-term
toxic
exposure
effect
of
PFOS
on
C.
quadricarinatus.
Three
environment
concentrations
(1
ng/L,
100
and
10
μg/L)
were
set
for
28
days
The
results
indicated
was
detected
serum,
muscle,
hepatopancreas
quadricarinatus,
order
accumulation
levels
as
follows:
>
serum
muscle.
Furthermore,
transcriptomics
showed
function
differentially
expressed
genes
(DEGs)
groups
related
biological
processes,
metabolism,
organic
system,
immune
response.
Kyoto
Encyclopedia
Genes
Genomes
enrichment
analysis
DEGs
significantly
enriched
lysosome
signaling
pathway,
retinol
binding,
fructose
mannose
glutathione
etc.,
pathway
most
significant,
which
key
effects
In
recent
years,
the
industrial
substitution
of
long-chain
per-
and
polyfluoroalkyl
substances
(PFAS)
with
short-chain
alternatives
has
become
increasingly
prevalent,
resulting
in
widespread
environmental
detection
perfluorohexanesulfonic
acid
(PFHxS),
a
PFAS.
However,
there
remains
limited
information
about
potential
adverse
effects
PFHxS
at
concentrations
to
wildlife.
Here,
early
life
stage
zebrafish
(
Archives of Toxicology,
Journal Year:
2024,
Volume and Issue:
98(10), P. 3381 - 3395
Published: July 2, 2024
Abstract
Per-
and
polyfluoroalkyl
substances
(PFAS)
are
man-made
chemicals
used
in
many
industrial
applications.
Exposure
to
PFAS
is
associated
with
several
health
risks,
including
a
decrease
infant
birth
weight,
hepatoxicity,
disruption
of
lipid
metabolism,
decreased
immune
response.
We
the
vitro
cell
models
screen
six
less
studied
[perfluorooctane
sulfonamide
(PFOSA),
perfluoropentanoic
acid
(PFPeA),
perfluoropropionic
(PFPrA),
6:2
fluorotelomer
alcohol
(6:2
FTOH),
sulfonic
FTSA),
8:2
(8:2
FTSA)]
for
their
capacity
activate
nuclear
receptors
cause
differential
expression
genes
involved
metabolism.
Cytotoxicity
assays
were
run
parallel
exclude
that
observed
gene
was
due
cytotoxicity.
Based
on
cytotoxicity
studies,
PFOSA
shown
be
more
potent
than
other
tested
PFAS.
crucial
bile
synthesis
detoxification,
cholesterol
synthesis,
transport,
metabolism
regulation.
Except
FTOH
FTSA,
all
downregulated
PPARA
expression.
The
reporter
assay
also
showed
FTSA
transactivated
farnesoid
X
receptor
(FXR).
this
study,
PFOSA,
prioritized
further
studies
confirm
understand
possible
effects
hepatic