Biomolecules,
Journal Year:
2021,
Volume and Issue:
11(9), P. 1292 - 1292
Published: Aug. 31, 2021
Manganese
(Mn)
is
an
essential
metal,
which
at
high
exposures
causes
neurotoxic
effects
and
neurodegeneration.
The
of
Mn
are
mediated
by
neuroinflammation,
oxidative
endoplasmic
reticulum
stress,
mitochondrial
dysfunction,
other
mechanisms.
Recent
findings
have
demonstrated
the
potential
impact
overexposure
on
gut
microbiota
dysbiosis,
known
to
contribute
neurodegeneration
via
secretion
neuroactive
proinflammatory
metabolites.
Therefore,
in
this
review,
we
discuss
existing
data
exposure
biodiversity,
bacterial
metabolite
production,
wall
permeability
regulating
systemic
levels.
that
may
affect
biodiversity
altering
abundance
Shiegella,
Ruminococcus,
Dorea,
Fusicatenibacter,
Roseburia,
Parabacteroides,
Bacteroidetes,
Firmicutes,
Ruminococcaceae,
Streptococcaceae,
phyla.
A
Mn-induced
increase
Bacteroidetes
a
reduced
Firmicutes/Bacteroidetes
ratio
lipopolysaccharide
Moreover,
addition
increased
(LPS)
levels,
capable
potentiating
LPS
neurotoxicity.
Due
metabolic
activity
intestinal
microflora,
perturbations
result
significant
alteration
metabolome
has
least
partially
mediate
biological
overexposure.
At
same
time,
recent
study
healthy
microbiome
transplantation
alleviates
neurotoxicity,
indicative
role
microflora
cascade
Mn-mediated
High
doses
cause
enterocyte
toxicity
integrity
through
disruption
tight
junctions.
resulting
further
promotes
translocation
metabolites
blood
flow,
ultimately
gaining
access
brain
leading
neuroinflammation
neurotransmitter
imbalance.
lead
us
hypothesize
should
be
considered
as
target
toxicity,
although
more
detailed
studies
required
characterize
interplay
between
gut,
well
its
pathogenesis
diseases.
Ecotoxicology and Environmental Safety,
Journal Year:
2023,
Volume and Issue:
253, P. 114616 - 114616
Published: Feb. 15, 2023
Manganese
(Mn)
accumulates
in
the
central
nervous
system
and
can
cause
neurotoxicity,
but
mechanisms
of
Mn-induced
neurotoxicity
remain
unclear.
We
performed
single-cell
RNA
sequencing
(scRNA-seq)
zebrafish
brain
after
Mn
exposure
identified
10
cell
types
by
marker
genes:
cholinergic
neurons,
dopaminergic
(DA)
glutaminergic
GABAergic
neuronal
precursors,
other
microglia,
oligodendrocyte,
radial
glia,
undefined
cells.
Each
type
has
its
distinct
transcriptome
profile.
Pseudotime
analysis
revealed
that
DA
neurons
had
a
critical
role
neurological
damage.
Combined
with
metabolomic
data,
chronic
significantly
impaired
amino
acid
lipid
metabolic
processes
brain.
Furthermore,
we
found
disrupted
ferroptosis
signaling
pathway
zebrafish.
Overall,
our
study
employed
joint
multi-omics
is
novel
potential
mechanism
neurotoxicity.
Biomolecules,
Journal Year:
2021,
Volume and Issue:
11(9), P. 1292 - 1292
Published: Aug. 31, 2021
Manganese
(Mn)
is
an
essential
metal,
which
at
high
exposures
causes
neurotoxic
effects
and
neurodegeneration.
The
of
Mn
are
mediated
by
neuroinflammation,
oxidative
endoplasmic
reticulum
stress,
mitochondrial
dysfunction,
other
mechanisms.
Recent
findings
have
demonstrated
the
potential
impact
overexposure
on
gut
microbiota
dysbiosis,
known
to
contribute
neurodegeneration
via
secretion
neuroactive
proinflammatory
metabolites.
Therefore,
in
this
review,
we
discuss
existing
data
exposure
biodiversity,
bacterial
metabolite
production,
wall
permeability
regulating
systemic
levels.
that
may
affect
biodiversity
altering
abundance
Shiegella,
Ruminococcus,
Dorea,
Fusicatenibacter,
Roseburia,
Parabacteroides,
Bacteroidetes,
Firmicutes,
Ruminococcaceae,
Streptococcaceae,
phyla.
A
Mn-induced
increase
Bacteroidetes
a
reduced
Firmicutes/Bacteroidetes
ratio
lipopolysaccharide
Moreover,
addition
increased
(LPS)
levels,
capable
potentiating
LPS
neurotoxicity.
Due
metabolic
activity
intestinal
microflora,
perturbations
result
significant
alteration
metabolome
has
least
partially
mediate
biological
overexposure.
At
same
time,
recent
study
healthy
microbiome
transplantation
alleviates
neurotoxicity,
indicative
role
microflora
cascade
Mn-mediated
High
doses
cause
enterocyte
toxicity
integrity
through
disruption
tight
junctions.
resulting
further
promotes
translocation
metabolites
blood
flow,
ultimately
gaining
access
brain
leading
neuroinflammation
neurotransmitter
imbalance.
lead
us
hypothesize
should
be
considered
as
target
toxicity,
although
more
detailed
studies
required
characterize
interplay
between
gut,
well
its
pathogenesis
diseases.