Cell Biology and Toxicology,
Journal Year:
2024,
Volume and Issue:
40(1)
Published: Aug. 20, 2024
Cell
death
maintains
cell
morphology
and
homeostasis
during
development
by
removing
damaged
or
obsolete
cells.
The
concentration
of
metal
ions
whithin
cells
is
regulated
various
intracellular
transporters
repositories
to
maintain
dynamic
balance.
External
internal
stimuli
might
increase
the
ions,
which
results
in
overloading.
Abnormal
accumulation
large
amounts
can
lead
disruption
signaling
cell,
turn
produce
toxic
effects
occurrence
different
types
deaths.
In
order
further
study
overloading
induced
death,
this
paper
reviewed
regulation
Ca2+,
Fe3+,
Cu2+
Zn2+
mechanism
Furthermore,
we
found
that
possess
a
synergistic
competitive
relationship
death.
And
enhanced
level
oxidative
stress
was
present
all
processes
due
overloading,
possibly
combination
factors.
Therefore,
review
offers
theoretical
foundation
for
investigation
presents
innovative
insights
targeted
therapeutic
intervention.
•
Metal
disrupts
homeostasis,
affects
cause
via
reactive
oxygen
species
(ROS).
Different
have
relationships
regulating
Environmental Toxicology,
Journal Year:
2023,
Volume and Issue:
39(4), P. 2052 - 2063
Published: Dec. 14, 2023
Abstract
Imidacloprid
(IMI)
is
a
neonicotinoid
insecticide
with
the
highest
global
market
share,
and
IMI
exposure
in
environment
can
negatively
affect
many
nontarget
organisms
(a
general
term
for
affected
by
drugs
other
than
target
organisms).
Resveratrol
(RSV),
non‐flavonoid
polyphenolic
organic
compound
derived
from
peanuts,
grapes,
plants,
has
anti‐inflammatory
antioxidant
effects.
It
currently
unclear
how
RSV
protects
against
cell
damage
caused
IMI.
Therefore,
we
established
an
experimental
model
of
chicken
lymphocyte
lines
exposed
to
110
μg/mL
and/or
0.5
μM
24
h.
According
results,
markedly
raised
intracellular
reactive
oxygen
species
levels
diminished
activity
cellular
enzymes
(CAT,
SOD,
GPx),
leading
MDA
accumulation
decreased
T‐AOC.
JNK
,
ERK
P38
essential
components
mitogen‐activated
protein
kinase
(MAPK)
signaling
pathway,
were
also
expressed
more
when
was
present.
Additionally,
resulted
upregulation
mitochondrial
apoptosis
(
Caspase
3
9
Bax
Cyt‐c
)
necroptosis
8
RIPK1
RIPK3
MLKL
related
factors
expression,
downregulation
Bcl‐2
induction
cytokine
IL‐6
TNF‐α
IFN‐γ
expression.
The
combined
treatment
significantly
reduced
oxidative
stress
levels,
inhibited
MAPK
alleviated
IMI‐induced
apoptosis,
necroptosis,
immune
dysfunction.
To
summarize,
antagonized
dysfunction
inhibiting
ROS/MAPK
pathway.
