It
is
known
that
exposure
to
heavy
metals
such
as
lead
(Pb)
and
cadmium
(Cd)
has
several
adverse
effects,
particularly
on
the
human
reproductive
system.
Pb
Cd
have
been
associated
with
infertility
in
both
men
women.
In
pregnant
women,
they
spontaneous
abortion,
preterm
birth,
impairment
of
development
fetus.
Since
these
come
from
natural
anthropogenic
activities
their
harmful
effects
observed
even
at
levels
exposure,
remains
a
public
health
issue,
especially
for
system.
Given
this,
present
study
aimed
investigate
potential
follicular
fluid
(FF)
infertile
women
no-smokers
exposed
professional
reasons
or
living
rural
areas
near
landfills
waste
disposal
areas,
correlate
intrafollicular
presence
possible
alterations
ultrastructure
cumulus-oocyte
complexes
(COCs),
probably
responsible
infertility.
Blood
FF
were
measured
using
atomic
absorption
spectrometry.
COCs
corresponding
each
analyzed
subjected
ultrastructural
analyses
by
transmission
electron
microscopy.
We
demonstrated
first
time
(0.66
µg/dL
0.85
µg/dL)
(0.26
µg/L
-
0.41
µg/L)
could
be
morphological
oocyte
CCs
ultrastructure.
blood
(0.54
1.87
above
current
reference
values
established
guidelines
Agency
Toxic
Substances
Disease
Registry
(ATSDR)
Environmental
Protection
(EPA),
whereas
(1.28
3.98
below
ATSDR
we
believe
due
Cd,
if
cannot
exclude
additional
effect
Pb.
Our
results
highlighted
oocytes
affected
maturation
quality,
showed
scarcely
active
steroidogenic
elements.
Regressing
CCs,
cytoplasmic
alterations,
also
numerous.
According
Cd's
endocrine-disrupting
activity,
poor
activity
might
delayed
maturation.
So,
conclude
negatively
affect
fertilization,
embryo
development,
pregnancy,
compromising
competence
fertilization
directly
indirectly,
impairing
CC
inducing
apoptosis.
Journal of Toxicology and Environmental Health Part B,
Journal Year:
2023,
Volume and Issue:
26(8), P. 442 - 467
Published: Oct. 2, 2023
Drug-Induced
Liver
Injury
(DILI)
constitutes
hepatic
damage
attributed
to
drug
exposure.
DILI
may
be
categorized
as
hepatocellular,
cholestatic
or
mixed
and
might
also
involve
immune
responses.
When
occurs
in
dose-dependent
manner,
it
is
referred
intrinsic,
while
if
the
injury
spontaneously,
termed
idiosyncratic.
This
review
predominately
focused
on
idiosyncratic
liver
injury.
The
established
molecular
mechanisms
for
include
(1)
mitochondria
dysfunction,
(2)
increased
reactive
oxygen
species
levels,
(3)
presence
of
elevated
apoptosis
necrosis,
(4)
bile
duct
injuries
associated
with
mediated
pathways.
However,
should
emphasized
that
underlying
responsible
are
still
unknown.
Prevention
strategies
critical
incidences
occur
frequently,
treatment
options
limited
once
has
developed.
aim
this
was
utilize
retrospective
cohort
studies
from
across
globe
gain
insight
into
epidemiological
patterns.
considers
what
currently
known
regarding
DILI,
discusses
potential
risk
factors
implications
coronavirus
pandemic
presentation
research.
Future
perspectives
considered
discussed
new
biomarkers,
causality
assessment
reporting
methods.
Future Journal of Pharmaceutical Sciences,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: March 28, 2025
Abstract
Background
Drug-induced
liver
injury
(DILI)
is
a
significant
adverse
drug
reaction,
manifesting
through
range
of
clinical
presentations
from
mild
enzyme
to
acute
failure.
Main
text
This
review
provides
comprehensive
overview
DILI,
emphasizing
the
differences
between
intrinsic
and
idiosyncratic
DILI.
The
underlying
molecular
mechanisms,
like
mitochondrial
dysfunction,
oxidative
stress,
immune-mediated
responses,
are
discussed
in
detail.
epidemiology
DILI
explored
various
retrospective
prospective
studies,
highlighting
role
specific
medications
individual
susceptibility
factors.
also
addresses
challenges
diagnosing
impact
on
development
practice.
Conclusion
poses
threat
due
its
potential
for
causing
failure
associated
mortality.
To
improve
patient
outcomes,
further
research
crucial
identify
effective
therapeutic
interventions.
Journal of Clinical and Translational Hepatology,
Journal Year:
2025,
Volume and Issue:
000(000), P. 000 - 000
Published: Jan. 21, 2025
Drug-induced
liver
injury
(DILI)
is
a
harmful
reaction
to
medications,
herbs,
and
dietary
supplements
that
results
in
dysfunction.
Based
on
the
distinct
clinical
patterns
of
damage,
DILI
can
be
categorized
into
hepatocellular,
cholestatic,
mixed
types.
Hepatocellular
linked
inflammation,
apoptosis,
necrosis,
while
cholestatic
commonly
associated
with
bile
plugs
and,
rare
cases,
ductopenia.
Ursodeoxycholic
acid
(UDCA)
therapeutic
agent
most
widely
used
for
treatment
hepatopathies
diverse
etiologies
has
been
mainly
as
supportive
DILI.
In
this
review,
we
presented
more
structured
systematic
framework
potential
application
hepatoprotective
across
broader
range
scenarios.
A
MEDLINE
search
literature
from
1995
present
retrieved
41
preliminary
studies
suggesting
UDCA
may
offer
curative
preventive
benefits
hepatocellular
well.
This
aligns
preclinical
rodents,
showing
beneficial
effects
experimental
irrespective
involved.
could
due
broad
potentially
UDCA,
which
address
various
types
damage
different
causes
mechanisms
seen
all
forms
UDCA's
properties
include
anticholestatic,
antioxidant,
anti-inflammatory,
anti-apoptotic,
anti-necrotic,
mitochondrial
protective,
endoplasmic
reticulum
stress-relieving,
immunomodulatory
effects.
Controlled
use
standardized
causality
assessments
are
eagerly
awaited
properly
validate
Meanwhile,
hope
article
helps
clarify
systematize
versatile
safe
medication
toxicity.
Cell Stress and Chaperones,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 1, 2025
Endoplasmic
reticulum
(ER)
stress-associated
apoptosis
is
involved
in
various
liver
diseases,
including
fibrosis,
nonalcoholic
fatty
disease,
and
cirrhosis.
Hepatocytes
respond
to
ER
stress
by
eliciting
unfolded
protein
response
(UPR)
enhancing
autophagy.
Autophagy
a
pivotal
mechanism
for
sustaining
normal
function,
through
degradation
of
damaged
fragments
removal
abnormal
aggregates
the
lumen.
Failure
restore
homeostasis
via
autophagy
harmful
hepatocytes
contributes
apoptosis.
Recent
findings
indicated
that
C/EBP
homologous
(CHOP)
could
exacerbate
stress-related
down-regulating
autophagy,
but
underlying
remains
elusive.
To
investigate
impact
CHOP
on
stress-induced
rat
hepatocytes,
potential
molecular
mechanisms.
BRL-3A
cells
were
pre-treated
with
rapamycin
(RAP)
3-methyladenine,
then
treated
dithiothreitol
(DTT).
Growth
apoptotic
rates
detected
using
real-time
cellular
analysis
(RTCA)
flow
cytometry,
respectively.
molecule
levels
determined
western
blotting.
CHOP,
small
interfering
RNA,
lentivirus
vector
system
used
transfect
observe
gene
silencing
or
overexpression
Chromatin
immunoprecipitation
(ChIP)
was
confirm
whether
binds
directly
ATG12,
ATG5,
LC3
promotor
regions
undergoing
stress.
molecules
dramatically
upregulated
hepatocyte
augmented.
RAP
pre-treatment
significantly
reduced
DTT-induced
expression
molecules;
conversely,
3-MA
promoted
molecules.
Following
decreased
level
autophagy-associated
increased,
decreased.
However,
opposite
trends
observed
cells.
A
negative
regulation
upon
DTT
treatment
ChIP.
enhancement
during
inhibits
promotes
apoptosis;
however,
attenuate
Overexpression
aggravate