SSRN Electronic Journal,
Journal Year:
2022,
Volume and Issue:
unknown
Published: Jan. 1, 2022
Living
organisms
are
now
constantly
exposed
to
microplastics
and
nanoplastics
(MNPLs),
besides
their
huge
toxic
potential,
they
can
also
act
as
carriers
of
various
hazardous
elements
like
heavy
metals.
Therefore,
this
study
explored
possible
interactions
between
polystyrene
(PSMPLs)
two
metal
pollutants:
cadmium
chloride
(CdCl2)
silver
nitrate
(AgNO3).
To
better
understand
the
extent
biological
effects
caused
by
different
sizes
PSMPLs,
we
conducted
in
vivo
experiments
with
five
doses
(from
0.01
10
mM)
that
contained
particles
measuring
4,
10,
20
µm
size
on
Drosophila
larvae
adult
flies.
Additional
were
performed
exposing
flies
individual
metals
CdCl2
(0.5
AgNO3
mM),
well
combined
exposure
PSMPLs
(0.01,
these
metals,
an
attempt
gain
new
insight
into
health
risks
such
coexposure.
Using
transmission
electron
microscopy
imaging,
managed
visualize
journey
ingested
throughout
fly’s
body,
observing
plastics
intestinal
lumen,
cellular
uptake
gut
enterocytes,
passage
plastic
through
barrier
leak
hemolymph,
hemocytes.
Observations
detected
shape
changes
PSMPLs.
Egg-to-adult
viability
screening
revealed
no
significant
toxicity
upon
tested
materials,
however
induced
aggravated
genotoxic
effects,
including
damage,
genetic
intracellular
oxidative
stress
(ROS
generation),
smaller
sized
+
(cadmium
silver)
causing
greater
damage.
Environmental Science Nano,
Journal Year:
2022,
Volume and Issue:
9(5), P. 1845 - 1857
Published: Jan. 1, 2022
Micro-
and
nanoplastics
(MNPLs)
are
intentionally
produced
for
commercial
uses
(primary
MNPLs)
or
formed
from
environmentally
aged
plastics
(secondary
MNPLs).
Biology,
Journal Year:
2022,
Volume and Issue:
11(10), P. 1470 - 1470
Published: Oct. 8, 2022
Living
organisms
are
now
constantly
exposed
to
microplastics
and
nanoplastics
(MNPLs),
besides
their
toxic
potential,
they
can
also
act
as
carriers
of
various
hazardous
elements
such
heavy
metals.
Therefore,
this
study
explored
possible
interactions
between
polystyrene
(PSMPLs)
two
metal
pollutants:
cadmium
chloride
(CdCl
Cell Reports,
Journal Year:
2021,
Volume and Issue:
36(5), P. 109478 - 109478
Published: Aug. 1, 2021
Oxidative
stress
is
a
ubiquitous
cellular
challenge
implicated
in
aging,
neurodegeneration,
and
cancer.
By
studying
pathogenic
mutations
the
tumor
suppressor
BRCA2,
we
identify
general
mechanism
by
which
oxidative
restricts
mitochondrial
(mt)DNA
replication.
BRCA2
inactivation
induces
R-loop
accumulation
mtDNA
regulatory
region
diminishes
replication
initiation.
In
BRCA2-deficient
cells,
intracellular
reactive
oxygen
species
(ROS)
are
elevated,
ROS
scavengers
suppress
defects.
Conversely,
wild-type
cells
exposed
to
pharmacologic
or
genetic
manipulation
phenocopy
these
Mechanistically,
find
that
8-oxoguanine
caused
suffices
impair
recruitment
of
enzyme
RNaseH1
sites
accrual,
restricting
Thus,
impairs
function
cripple
maintenance.
Our
findings
highlight
molecular
links
dysfunction
elicited
genes
neurodegeneration
Genes and Environment,
Journal Year:
2023,
Volume and Issue:
45(1)
Published: July 1, 2023
Benzo(a)pyrene
(BaP),
the
earliest
and
most
significant
carcinogen
among
polycyclic
aromatic
hydrocarbons
(PAHs),
has
been
found
in
foods,
tobacco
smoke,
automobiles
exhaust,
etc.
Exposure
to
BaP
induced
DNA
damage
directly,
or
oxidative
stress-related
damage,
resulting
cell
apoptosis
carcinogenesis
human
respiratory
system,
digestive
reproductive
Moreover,
triggered
genome-wide
epigenetic
alterations
by
methylation,
which
might
cause
disturbances
regulation
of
gene
expression,
thereby
cancer.
It
proved
that
reduced
activated
proto-oncogene
hypomethylation
promoter
region,
but
silenced
tumor
suppressor
genes
hypermethylation,
cancer
initiation
progression.
Here
we
summarized
changes
methylation
exposure,
revealed
plays
a
role
development.
Pharmacological Research,
Journal Year:
2024,
Volume and Issue:
204, P. 107187 - 107187
Published: April 23, 2024
Cardiovascular
diseases
(CVD)
persist
as
a
prominent
cause
of
mortality
worldwide,
with
oxidative
stress
constituting
pivotal
contributory
element.
The
modification
guanosine,
specifically
8-oxoguanine,
has
emerged
crucial
biomarker
for
stress,
providing
novel
insights
into
the
molecular
underpinnings
CVD.
8-Oxoguanine
can
be
directly
generated
at
DNA
(8-oxo-dG)
and
RNA
levels,
well
free
nucleotide
level
(8-oxo-dGTP
or
8-oxo-GTP),
which
are
produced
integrated
through
replication
transcription.
When
exposed
to
guanine
is
more
readily
in
than
DNA.
A
burgeoning
body
research
surrounds
exhibits
its
accumulation
playing
role
development
Therapeutic
approaches
targeting
damage
RNA,
encompassing
modulation
repair
enzymes
small
molecule
inhibitors,
anticipated
enhance
CVD
management.
In
conclusion,
we
explore
noteworthy
elevation
8-oxoguanine
levels
patients
various
cardiac
conditions
deliberate
upon
formation
regulation
8-oxo-dG
8-oxo-G
under
their
function
DNA repair,
Journal Year:
2024,
Volume and Issue:
139, P. 103694 - 103694
Published: May 18, 2024
Multiple
separate
repair
mechanisms
safeguard
the
genome
against
various
types
of
DNA
damage,
and
their
failure
can
increase
rate
spontaneous
mutagenesis.
The
malfunction
distinct
leads
to
genomic
instability
through
different
mutagenic
processes.
For
example,
defective
mismatch
causes
high
base
substitution
rates
microsatellite
instability,
whereas
homologous
recombination
deficiency
is
characteristically
associated
with
deletions
chromosome
instability.
This
review
presents
a
comprehensive
collection
all
phenotypes
loss
each
mechanism,
drawing
on
data
from
variety
model
organisms
mutagenesis
assays,
placing
greatest
emphasis
systematic
analyses
human
cancer
datasets.
We
describe
latest
theories
mechanism
process,
often
explained
by
reliance
an
alternative
pathway
or
error-prone
replication
unrepaired,
damaged
DNA.
Aided
concept
mutational
signatures,
be
used
in
diagnosis
identify
pathways.
Nucleic Acids Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 31, 2024
Abstract
Cellular
senescence
plays
a
significant
role
in
tissue
aging.
Senescent
cells,
which
resist
apoptosis
while
remaining
metabolically
active,
generate
endogenous
DNA-damaging
agents,
primarily
reactive
oxygen
species.
Efficient
DNA
repair
is
therefore
crucial
these
especially
when
they
undergo
escape,
resuming
replication
and
cellular
proliferation.
To
investigate
whether
senescent
cell
transcriptomes
reflect
adequate
capacity,
we
conducted
comprehensive
meta-analysis
of
60
transcriptomic
datasets
comparing
to
proliferating
cells.
Our
analysis
revealed
striking
downregulation
genes
encoding
essential
components
across
pathways
This
includes
active
different
cycle
phases
such
as
nucleotide
excision
repair,
base
nonhomologous
end
joining
homologous
recombination
double-strand
breaks,
mismatch
interstrand
crosslink
repair.
The
observed
suggests
accumulation
lesions.
Experimental
monitoring
readouts
cells
that
underwent
radiation-induced
supported
this
conclusion.
phenomenon
was
consistent
various
triggers
also
primary
lines
from
aging
individuals.
These
findings
highlight
the
potential
‘ticking
bombs’
aging-related
diseases
tumors
recurring
following
therapy-induced
senescence.