Trichothecene
mycotoxin
T-2
toxin
is
an
important
environmental
pollutant
and
poses
a
global
threat
to
human
animal
health.
could
induce
nephrotoxicity,
however,
the
precise
molecular
mechanism
remains
unclear.
In
this
study,
mice
were
intraperitoneally
administrated
with
single
dose
of
2
mg/kg
toxin.
The
kidney
function
ultrastructural
observation
also
assessed
found
exposure
cause
damage.
Transmission
electron
microscopy
showed
significant
swelling
vacuolization
mitochondria
renal
cell.
A
total
1122,
58,
391
differential
expression
genes
(DEGs)
that
predominantly
expressed
in
tissues
at
1
d,
3
7
d
after
exposure,
respectively.
Early
transcriptomic
changes
down-regulation
DEGs
involved
cell
cycle,
p53
signaling
pathway,
cellular
senescence,
while
up-regulation
referred
ribosome
pathway.
temporal
variations
gene
pattern
presented
metabolism
was
disturbed
recovery
period
d.
conclusion,
for
first
time,
provided
comprehensive
comparative
analysis
regulation
exposure-induced
nephrotoxicity
different
periods
explored
mRNA
level.
Ecotoxicology and Environmental Safety,
Journal Year:
2023,
Volume and Issue:
270, P. 115844 - 115844
Published: Dec. 21, 2023
T-2
toxin
is
a
trichothecene
mycotoxin
of
significant
danger
to
humans
and
animals.
Its
impact
on
reproductive
toxicity
attributed
oxidative
stress,
which
ultimately
leads
cell
death.
Ferroptosis
programmed
death
that
characterized
by
lipid
peroxidation.
This
study
aimed
investigate
the
toxic
effects
mouse
testis
potential
mechanism
toxin-induced
ferroptosis.
significantly
altered
morphology
decreased
testosterone
level,
sperm
concentration,
increased
malformation
rate,
as
well
induced
damage
with
reactive
oxygen
species
malondialdehyde
accumulated,
activity
superoxide
dismutase,
glutathione
peroxidase
decreased.
Additionally,
ferroptosis
accumulating
iron
ions,
increasing
prostaglandin
endoperoxide
synthase
2,
downregulating
4
ferritin
heavy
chain
1,
manifesting
ferroptotic
morphological
alterations,
leading
testicular
impairment.
Administration
inhibitor
liproxstatin-1
or
antioxidant
resveratrol
effectively
mitigated
injury.
These
findings
provided
novel
insights
into
fundamental
furnished
further
proof
therapeutic
effect
in
addressing
Journal of Cardiovascular Pharmacology,
Journal Year:
2023,
Volume and Issue:
unknown
Published: Oct. 10, 2023
Ferroptosis
is
a
form
of
iron-regulated
cell
death
implicated
in
wide
array
diseases,
including
heart
failure,
hypertension,
and
numerous
cardiomyopathies.
In
addition,
mitochondrial
dysfunction
has
been
associated
with
several
these
same
disease
states.
However,
the
role
mitochondrion
ferroptotic
remains
debated.
As
major
regulator
cellular
iron
levels,
mitochondria
may
very
well
play
crucial
mechanisms
behind
ferroptosis,
but
at
this
point,
not
adequately
defined.
Emerging
evidence
from
our
laboratory
others
indicates
critical
Sirtuin
3,
deacetylase
linked
longevity
protection
against
conditions,
prevention
cardiovascular
diseases.
Here,
we
provide
brief
overview
potential
roles
3
homeostasis
its
contribution
to
cardiomyopathy
Friedreich's
ataxia
diabetic
cardiomyopathy.
We
also
discuss
current
knowledge
involvement
ferroptosis
other
states,
doxorubicin-induced
cardiomyopathy,
insight
into
areas
requiring
further
investigation.
Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
284, P. 116909 - 116909
Published: Aug. 22, 2024
T-2
toxin,
a
trichothecene
mycotoxin,
is
an
important
environmental
pollutant
that
poses
threat
globally
to
the
health
of
humans
and
animals.
It
has
been
found
induce
nephrotoxicity;
however,
precise
molecular
mechanism
involved
remains
unclear.
In
this
study,
mice
were
administered
at
single
dose
2
mg/kg
body
weight
toxin
intraperitoneally,
kidney
function
ultrastructural
observations
assessed
after
1
d,
3
7
d.
Histopathological
findings
revealed
exposure
caused
noticeable
tubular
degeneration,
necrosis
epithelial
cell
shedding
in
mouse
kidneys.
Transmission
electron
microscopy
indicated
mitochondrial
swelling
vacuolization.
Transcriptomic
data
significant
differences
expression
1122,
58,
391
genes
tissues
or
d
exposure,
respectively.
Moreover,
downregulated
differentially
expressed
(DEGs)
be
cycle,
p53
signaling,
cellular
senescence
pathways,
while
upregulated
DEGs
associated
with
ribosomal
pathway.
Temporal
changes
gene
patterns
(i.e.,
d)
disturbances
metabolism
during
recovery
period
(7
detected
kidneys
toxin.
conclusion,
study
first
provide
comprehensive
comparative
transcriptomic
analysis
exposure-induced
nephrotoxicity-related
regulation
different
time
points
investigate
underlying
nephrotoxicity
mRNA
level.
