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
Perfluorooctane
sulfonamide
(PFOSA)
is
an
immediate
perfluorooctanesulfonate
(PFOS)
precursor
(PreFOS).
Previous
studies
have
shown
PFOSA
to
induce
stronger
toxic
responses
compared
other
perfluorinated
compounds
(PFCs).
However,
the
specific
nature
of
PFOSA-induced
toxicity,
whether
autonomous
or
mediated
by
its
metabolite
PFOS,
has
not
been
fully
elucidated.
This
study
systematically
investigates
immunomodulatory
effects
and
PFOS
in
zebrafish
(
Toxicity
mechanisms
of
per-
and
polyfluoroalkyl
substances
(PFAS),
a
chemical
class
present
in
diverse
ecosystems,
are
not
well
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,
locomotor
activity,
gene
expression
zebrafish
embryos
larvae
following
continuous
exposure
PFOSA
beginning
at
6
hours
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
affect
hatch
rate,
nor
it
induce
reactive
oxygen
species
7-day-old
fish.
However,
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
transcript
levels
acetylcholinesterase
(ache),
elav-like
RNA
binding
protein
3
(elavl3),
growth
43
(gap43),
synapsin
II
(syn2a),
tubulin
(tubb3)
all
increased
higher
exposure.
This
study
contributes
our
knowledge
regarding
toxicity
data
future
risk
assessment
strategies
these
concerning,
persistent
environmental
pollutants.
Perfluorooctane
sulfonate
(PFOS)
and
its
precursor,
perfluorooctane
sulfonamide
(PFOSA),
are
widespread
in
the
environment.
Evidence
suggests
a
strong
link
between
maternal
exposure
to
PFOS/PFOSA
congenital
heart
diseases
offspring,
but
mechanisms
remain
unclear.
We
hypothesized
that
PFOS
PFOSA
induce
cardiac
defects
through
peroxisome
proliferator-activated
receptor
gamma
(PPARγ)
aryl
hydrocarbon
(AHR)
pathways,
respectively.
In
this
study,
we
demonstrated
exposing
zebrafish
embryos
either
or
caused
malformations
dysfunction.
Both
induced
reactive
oxygen
species
(ROS)
overproduction,
mitochondrial
damage,
apoptosis
embryonic
hearts.
Blockade
of
PPARγ
pharmaceutical
inhibitor
genetic
knockdown
only
attenuated
changes
by
PFOS,
not
PFOSA.
Conversely,
inhibition
AHR
alleviated
adverse
effects
PFOS.
exhibited
similar
binding
affinities
molecular
docking.
The
varying
ability
activity
hearts
can
be
attributed
their
different
capabilities
for
activating
PPARγ.
summary,
our
findings
indicate
excessive
ROS
production
via
This
oxidative
stress
causes
damage
apoptosis,
leading
defects.
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
