N-(1,3-Dimethylbutyl)-N′-phenyl-1,4-phenylenediamine
(6PPD)
and
its
oxidation
product
6PPD-quinone
(6PPDQ)
showed
different
acute
toxicities
bioaccumulation
potencies
in
fish.
In
this
study,
we
compared
the
thyroid
disrupting
effects
of
6PPD
6PPDQ
through
vitro,
silico,
vivo
assays.
Interestingly,
although
similar
docking
affinities
with
hormone
receptor
(TR)
isoforms
GH3
cell
inhibition
effects,
signaling
pathway,
eye
development,
phototactic
behaviors,
density
retinal
layer
larval
zebrafish
were
significantly
affected
only
following
exposure.
Further
investigation
demonstrates
that
can
act
as
a
TR
antagonist
to
reduce
opsin
protein
abundance
inhibit
cone
photoreceptor
proliferation,
which
finally
alters
structure
causes
microphthalmus
zebrafish.
Especially,
under
environmental
relevant
concentration
exposure,
induced
alterations
trβ,
opn1lw1,
opn1mw1,
rpe65a,
nr2e3
gene
expressions
no
significant
histopathological
change
was
observed.
This
study
illustrates
for
first
time
more
serious
visual
system
impairment
6PPDQ,
disruption
being
contributing
factor,
while
other
important
toxic
targets
still
require
further
research.
Toxics,
Journal Year:
2025,
Volume and Issue:
13(1), P. 53 - 53
Published: Jan. 12, 2025
A
considerable
quantity
of
microplastic
debris
exists
in
the
environment
and
toxicity
these
materials
has
a
notable
impact
on
aquatic
ecosystems.
In
this
paper,
50–500
µm
polystyrene
microplastics
(exposure
concentrations
were
200
µg/L,
800
3200
µg/L
concentrations)
selected
to
study
effects
(PS-MPs)
cell
morphology,
detoxification
enzyme
activity,
mRNA
expression
liver
tissues
crucian
carp
juveniles.
The
results
demonstrated
that:
(1)
Different
PS-MPs
cause
varying
degrees
pathological
oxidative
damage
tissue
cells
carp.
higher
concentration
microplastics,
lower
antioxidant
(CAT,
GST,
SOD)
activity
greater
damage.
These
demonstrate
typical
dose–effect
relationship.
(2)
Principal
component
analysis
Spearman’s
correlation
that
four
components,
namely
glutathione
S-transferase
(GST)
its
related
genes
(GSTpi,
GSTα),
along
with
catalase
(CAT),
contributed
most
observed
outcome.
components
relatively
high
level
responsiveness
PS-MP
exposure
can
be
employed
as
ecotoxicological
indicators
microplastics.
(3)
This
experiment
evaluated
five
three
treatments,
which
found
had
different
gene
tested
involved
response
pathways
associated
virulence.
study,
was
determined
at
cellular,
protein,
levels,
combined
principal
identify
sensitivity
provide
scientific
basis
for
ecological
risk
assessment
safe
use
Fishes,
Journal Year:
2025,
Volume and Issue:
10(4), P. 146 - 146
Published: March 25, 2025
N-(1,3-dimethylbutyl)-N’-phenyl-p-benzoquinone
(6PPD-Q)
is
an
emerging
environmental
contaminant
that
widely
distributed
in
aquatic
environments
and
presents
significant
toxicological
risks
to
organisms.
As
6PPD-Q
primarily
derived
from
oxidative
transformation
of
the
tire
antioxidant
N-(1,3-dimethylbutyl)-N’-phenyl-p-phenylenediamine
(6PPD),
its
persistence
potential
for
bioaccumulation
organisms
have
raised
widespread
concerns.
This
study
reviews
sources,
spatial
distribution,
migration,
behaviors
6PPD-Q,
as
well
degradation
mechanisms
different
media.
Additionally,
this
review
systematically
explores
effects
on
organisms,
including
physiological,
biochemical,
molecular
impacts
fish,
crustaceans,
mollusks,
algae,
with
a
focus
mechanisms.
Finally,
we
discuss
limitations
current
research
propose
key
directions
future
studies,
long-term
ecological
risk
assessments,
bioaccumulation,
metabolic
pathway
analysis,
optimization
pollution
control
strategies,
aiming
provide
scientific
basis
assessment
management
6PPD-Q.
Distinct
from
other
nontoxic
phenyl-p-phenylenediamine
(PPD)
quinones,
N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone
(6PPD-Q)
was
recently
discovered
to
be
regioselectively
metabolized
alkyl
hydroxylated
metabolites
(alkyl-OH-6PPD-Q)
in
rainbow
trout.
It
remains
unknown
whether
the
unique
alkyl-OH-6PPD-Q
contributes
toxicity
of
6PPD-Q.
To
test
this,
we
herein
synthesized
chemical
standards
isomers
and
investigated
their
metabolic
formation
mechanism
toxicity.
The
predominant
confirmed
on
C4
tertiary
carbon
(C4-OH-6PPD-Q).
C4-OH-6PPD-Q
only
observed
microsomal
but
not
cytosolic
fractions
trout
(O.
mykiss)
liver
S9.
A
general
cytochrome
P450
(CYP450)
inhibitor
fluoxetine
inhibited
6PPD-Q,
supporting
that
CYP450
catalyzed
hydroxylation.
This
well-explained
compound-
regio-selective
C4-OH-6PPD-Q,
due
weak
C-H
bond
carbon.
Surprisingly,
while
cytotoxicity
for
6PPD-Q
C3-OH-6PPD-Q
a
coho
salmon
kisutch)
embryo
(CSE-119)
cell
line,
no
C4-OH-6PPD-Q.
further
confirm
this
under
physiologically
relevant
conditions,
fractionated
formed
microsome
Cytotoxicity
fraction
In
summary,
study
highlighted
as
key
moiety
both
metabolism
hydroxylation
is
detoxification
pathway
