Chemical Research in Toxicology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 8, 2025
The
usage
of
cobalt
(Co)
and
nickel
(Ni)
in
numerous
commercial,
industrial,
military
applications
causes
widespread
exposure
nowadays,
concerns
are
rising
about
adverse
impacts
on
human
health.
Emphasis
is
the
respiratory
system,
with
both
metals
classified
as
(possibly)
carcinogenic
upon
inhalation
by
International
Agency
for
Research
Cancer
(IARC),
but
limited
data
available
oral
exposure.
Therefore,
this
study
aims
to
evaluate
vitro
genotoxicity
Co(II)
Ni(II)
their
combination
HepG2
cells,
since
those
environmental
pollutants
occurs
realistically
concert.
Here,
led
induction
single-strand
breaks
oxidative
DNA
damage
detected
Comet
assay
FPG-sensitive
sites,
while
increased
abundance
γ-H2AX,
an
indicator
double-strand
breaks.
Notably,
combined
resulted
enhanced
damage,
especially
at
chromosomal
level,
formation
micronuclei
well
polynucleated
indicating
a
stronger
effect
compared
single
Furthermore,
induced
response
pathway
PARylation.
As
process
involves
consumption
large
amounts
cellular
NAD+
after
energy
state
was
assessed
Ni(II).
Current
indicate
that
altered
state.
This
reveals
distinct
mechanisms
exhibited
Ni(II),
which
were
treatment.
highlights
need
further
research
estimate
genotoxic
potential
targeting
cells
intake
increasing
entry.
Chemosphere,
Год журнала:
2024,
Номер
357, С. 142091 - 142091
Опубликована: Апрель 20, 2024
The
two
trace
elements
cobalt
(Co)
and
nickel
(Ni)
are
widely
distributed
in
the
environment
due
to
increasing
industrial
application,
for
example
lithium-ion
batteries.
Both
metals
known
cause
detrimental
health
impacts
humans
when
overexposed
both
supposed
be
a
risk
factor
various
diseases.
individual
toxicity
of
Co
Ni
has
been
partially
investigated,
however
underlying
mechanisms,
as
well
interactions
remain
unknown.
In
this
study,
we
focused
on
treatment
liver
carcinoma
(HepG2)
astrocytoma
(CCF-STTG1)
cells
model
target
sites
these
metals.
We
investigated
their
effects
single
combined
exposure
cell
survival,
death
bioavailability,
induction
oxidative
stress.
combination
CoCl2
NiCl2
resulted
higher
levels
with
subsequent
decreased
amount
compared
treatment.
Only
led
RONS
increased
GSSG
formation,
while
apoptosis
necrosis
seem
involved
mechanisms
NiCl2.
Collectively,
study
demonstrates
cell-type
specific
toxicity,
HepG2
representing
more
sensitive
line.
Importantly,
is
toxic
than
exposure,
which
may
originate
partly
from
respective
cellular
content.
Our
data
imply
that
major
mechanism
joint
associated
More
studies
needed
assess
after
such
advance
an
improved
hazard
prediction
less
artificial
real-life
scenarios.
Chemical Research in Toxicology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 8, 2025
The
usage
of
cobalt
(Co)
and
nickel
(Ni)
in
numerous
commercial,
industrial,
military
applications
causes
widespread
exposure
nowadays,
concerns
are
rising
about
adverse
impacts
on
human
health.
Emphasis
is
the
respiratory
system,
with
both
metals
classified
as
(possibly)
carcinogenic
upon
inhalation
by
International
Agency
for
Research
Cancer
(IARC),
but
limited
data
available
oral
exposure.
Therefore,
this
study
aims
to
evaluate
vitro
genotoxicity
Co(II)
Ni(II)
their
combination
HepG2
cells,
since
those
environmental
pollutants
occurs
realistically
concert.
Here,
led
induction
single-strand
breaks
oxidative
DNA
damage
detected
Comet
assay
FPG-sensitive
sites,
while
increased
abundance
γ-H2AX,
an
indicator
double-strand
breaks.
Notably,
combined
resulted
enhanced
damage,
especially
at
chromosomal
level,
formation
micronuclei
well
polynucleated
indicating
a
stronger
effect
compared
single
Furthermore,
induced
response
pathway
PARylation.
As
process
involves
consumption
large
amounts
cellular
NAD+
after
energy
state
was
assessed
Ni(II).
Current
indicate
that
altered
state.
This
reveals
distinct
mechanisms
exhibited
Ni(II),
which
were
treatment.
highlights
need
further
research
estimate
genotoxic
potential
targeting
cells
intake
increasing
entry.
