Environmental Science & Technology,
Journal Year:
2024,
Volume and Issue:
58(2), P. 1022 - 1035
Published: Jan. 2, 2024
There
is
epidemiological
evidence
in
humans
that
exposure
to
endocrine-disrupting
chemicals
such
as
bisphenol
A
(BPA)
tied
abnormal
neuroendocrine
function
with
both
behavioral
and
intestinal
symptoms.
However,
the
underlying
mechanism
of
this
effect,
particularly
role
gut–brain
regulation,
poorly
understood.
We
exposed
zebrafish
embryos
a
concentration
series
(including
environmentally
relevant
levels)
BPA
its
analogues.
The
analogue
G
(BPG)
yielded
strongest
impact
on
larvae
inhibited
largest
number
neurotransmitters,
an
effective
0.5
μg/L,
followed
by
AF
(BPAF)
BPA.
In
neurod1:EGFP
transgenic
zebrafish,
BPG
BPAF
distribution
enteroendocrine
cells
(EECs),
which
associated
decreased
neurotransmitters
level
activity.
Immune
staining
ace-α-tubulin
suggested
vagal
neural
development
at
50
500
μg/L.
Single-cell
RNA-Seq
demonstrated
disrupted
system
inducing
inflammatory
responses
epithelial
via
TNFα-trypsin-EEC
signaling.
activated
apoptosis
developmental
pathways
neurons,
consistent
immunofluorescence
imaging
studies.
These
findings
show
affect
through
axis
but
different
mechanisms,
revealing
new
insights
into
modes
bisphenol-mediated
disruption.
