BioEssays,
Journal Year:
2024,
Volume and Issue:
46(7)
Published: May 7, 2024
Flavin-containing
monooxygenases
(FMOs),
traditionally
known
for
detoxifying
xenobiotics,
are
now
recognized
their
involvement
in
endogenous
metabolism.
We
recently
discovered
that
an
isoform
of
FMO,
fmo-2
Caenorhabditis
elegans,
alters
metabolism
to
impact
longevity
and
stress
tolerance.
Increased
expression
C.
elegans
modifies
the
flux
through
key
pathway
as
One
Carbon
Metabolism
(OCM).
This
modified
results
a
decrease
ratio
S-adenosyl-methionine
(SAM)
S-adenosyl-homocysteine
(SAH),
consequently
diminishing
methylation
capacity.
Here
we
discuss
how
FMO-2-mediated
formate
production
during
tryptophan
may
serve
trigger
changing
OCM.
suggest
bridges
OCM,
altering
metabolic
away
from
overexpression.
Additionally,
highlight
these
intersect
with
mTOR
AMPK
pathways,
addition
mitochondrial
In
conclusion,
goal
this
essay
is
bring
attention
central
role
FMO
enzymes
but
lack
understanding
mechanisms.
justify
call
deeper
enzyme's
rewiring
tryptophan/formate
or
other
yet
unidentified
substrates.
emphasize
identification
novel
drugs
microbes
induce
activity
extend
lifespan.
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(3), P. 652 - 652
Published: March 6, 2023
Neurotoxicity
is
induced
by
different
toxic
substances,
including
environmental
chemicals,
drugs,
and
pathogenic
toxins,
resulting
in
oxidative
damage
neurodegeneration
mammals.
The
nervous
system
extremely
vulnerable
to
stress
because
of
its
high
oxygen
demand.
Mitochondria
are
the
main
source
ATP
production
brain
neuron,
stress-caused
mitochondrial
dysfunction
implicated
neurodegenerative
diseases.
H2S
was
initially
identified
as
a
gas;
however,
more
recently,
it
has
been
recognized
neuromodulator
well
neuroprotectant.
Specifically,
modulates
activity,
oxidation
mitochondria
produces
various
reactive
sulfur
species,
thus
modifying
proteins
through
sulfhydration.
This
review
focused
on
highlighting
neuron
modulation
role
regulating
diseases
anti-oxidative,
anti-inflammatory,
anti-apoptotic
S-sulfhydration,
emphasized
importance
therapeutic
molecule
for
neurological
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Jan. 7, 2025
Sodium
aescinate
(SA),
a
natural
plant
extract
with
various
bioactivities,
is
widely
used
to
treat
oedema
and
inflammation
in
clinics.
However,
adverse
events,
including
liver
injury,
kidney
phlebitis,
have
been
reported
patients
SA
recent
years.
In
this
study,
we
BALB/c
mice
L02
cells
evaluate
the
role
of
ferroptosis
SA-induced
injury.
significantly
increased
AST,
ALT,
MDA
Fe2+,
decreased
GSH
levels,
induced
pathological
changes
vivo.
also
reduced
viability
LDH
release,
intracellular
cysteine
reduction,
depletion,
iron
accumulation,
ROS
production,
lipid
peroxidation,
indicating
that
causes
ferroptosis.
addition,
inhibited
transcriptional
activity
activating
transcription
factor
4
(ATF4)
subsequently
expression
downstream
genes
xCT
(solute
carrier
family
7a
member
11,
SLC7A11)
Cystathionine
gamma-lyase
(CTH)
which
play
vital
roles
biosynthesis.
Interestingly,
cytotoxic
effects
were
effectively
attenuated
by
ATF4
overexpression,
while
they
aggravated
silencing.
These
results
revealed
triggers
hepatocyte
inhibiting
ATF4,
an
oxidative
imbalance.
Pharmacological Research,
Journal Year:
2024,
Volume and Issue:
203, P. 107180 - 107180
Published: April 9, 2024
Primary
mitochondrial
diseases
(PMD)
are
amongst
the
most
common
inborn
errors
of
metabolism
causing
fatal
outcomes
within
first
decade
life.
With
marked
heterogeneity
in
both
inheritance
patterns
and
physiological
manifestations,
these
conditions
present
distinct
challenges
for
targeted
drug
therapy,
where
effective
therapeutic
countermeasures
remain
elusive
clinic.
Hydrogen
sulfide
(H2S)-based
therapeutics
may
offer
a
new
option
patient
treatment,
having
been
proposed
as
conserved
substrate
post-translational
regulator
across
species,
displaying
effects
age-related
dysfunction
neurodegenerative
models
disease.
H2S
can
stimulate
respiration
at
sites
downstream
PMD-defective
subunits,
augmenting
energy
production,
function
reducing
cell
death.
Here,
we
highlight
primary
signalling
mechanisms
mitochondria
relevant
PMD
outline
key
cytoprotective
proteins/pathways
amenable
to
restoration
via
H2S-mediated
persulfidation.
The
here,
combined
with
advent
potent
mitochondria-targeted
delivery
molecules,
could
provide
framework
countermeasure
disease
progression.
