Antioxidants,
Journal Year:
2022,
Volume and Issue:
11(2), P. 235 - 235
Published: Jan. 26, 2022
The
raising
prevalence
of
obesity
is
associated
with
an
increased
risk
for
cardiovascular
diseases
(CVDs),
particularly
coronary
artery
disease
(CAD),
and
heart
failure,
including
atrial
fibrillation,
ventricular
arrhythmias
sudden
death.
Obesity
contributes
directly
to
incident
factors,
hyperglycemia
or
diabetes,
dyslipidemia,
hypertension,
which
are
involved
in
atherosclerosis,
structural
functional
cardiac
alterations,
lead
dysfunction.
CVDs
the
main
cause
morbidity
mortality
worldwide.
In
obesity,
visceral
epicardial
adipose
tissue
generate
inflammatory
cytokines
reactive
oxygen
species
(ROS),
induce
oxidative
stress
contribute
pathogenesis
CVDs.
Nuclear
factor
erythroid
2-related
2
(NRF2;
encoded
by
Nfe2l2
gene)
protects
against
electrophilic
stress.
NRF2
participates
regulation
cell
responses
lipid
metabolism,
expression
over
1000
genes
under
normal
stressed
environments.
downregulated
inflammation.
knockout
mice
develop
deficiency
macrophages
increases
atherosclerosis.
Given
endothelial
protective
effects
experimental
models,
its
activation
using
pharmacological
natural
products
a
promising
therapeutic
approach
This
review
provides
comprehensive
summary
current
knowledge
on
role
obesity-associated
factors.
ACS Nano,
Journal Year:
2017,
Volume and Issue:
11(6), P. 6211 - 6217
Published: May 10, 2017
We
developed
a
high-efficiency
rotating
triboelectric
nanogenerator
(R-TENG)
enhanced
polyimide
(PI)
nanofiber
air
filter
for
particulate
matter
(PM)
removal
in
ambient
atmosphere.
The
PI
electrospinning
film
exhibited
high
efficiency
the
PM
particles
that
have
diameters
larger
than
0.5
μm.
When
R-TENG
is
connected,
of
enhanced,
especially
when
particle
are
smaller
100
nm.
highest
90.6%
with
diameter
33.4
nm
and
enhancement
reaches
207.8%
at
76.4
where
from
27.1%
to
83.6%.
This
technology
zero
ozone
release
low
pressure
drop
offers
an
approach
cleaning
haze
treatment.
International Journal of Environmental Research and Public Health,
Journal Year:
2021,
Volume and Issue:
18(10), P. 5227 - 5227
Published: May 14, 2021
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
one
of
the
most
frequent
causes
chronic
in
Western
world,
probably
due
to
growing
prevalence
obesity,
metabolic
diseases,
and
exposure
some
environmental
agents.
In
certain
patients,
simple
hepatic
steatosis
can
progress
non-alcoholic
steatohepatitis
(NASH),
which
sometimes
lead
cirrhosis
its
complications
including
hepatocellular
carcinoma.
Understanding
mechanisms
that
cause
progression
NAFLD
NASH
crucial
be
able
control
advancement
disease.
The
main
hypothesis
considers
it
multiple
factors
act
together
on
genetically
predisposed
subjects
suffer
from
insulin
resistance,
nutritional
factors,
gut
microbiota,
genetic
epigenetic
factors.
this
article,
we
will
discuss
epidemiology
NAFLD,
overview
several
topics
influence
development
possible
complications.
Journal of Thoracic Disease,
Journal Year:
2017,
Volume and Issue:
9(11), P. 4398 - 4412
Published: Nov. 1, 2017
Background:
Particulate
matter
(PM)
is
a
high
risk
factor
for
various
respiratory
diseases
and
triggers
an
inflammatory
response
in
lung
tissues.
However,
the
molecular
mechanism
of
PM-induced
incompletely
understood.
Free Radical Biology and Medicine,
Journal Year:
2020,
Volume and Issue:
151, P. 69 - 87
Published: Jan. 7, 2020
Cardiovascular
causes
have
been
estimated
to
be
responsible
for
more
than
two
thirds
of
the
considerable
mortality
attributed
air
pollution.
There
is
now
a
substantial
body
research
demonstrating
that
exposure
pollution
has
many
detrimental
effects
throughout
cardiovascular
system.
Multiple
biological
mechanisms
are
responsible,
however,
oxidative
stress
prominent
observation
at
levels
impairment
induced
by
pollutant
exposure.
This
review
provides
an
overview
evidence
key
pathway
different
actions
Particle and Fibre Toxicology,
Journal Year:
2018,
Volume and Issue:
15(1)
Published: Jan. 12, 2018
Epidemiological
studies
have
shown
that
ambient
air
pollution
is
closely
associated
with
increased
respiratory
inflammation
and
decreased
lung
function.
Particulate
matters
(PMs)
are
major
components
of
damages
cells.
However,
the
mechanisms
remain
to
be
elucidated.
This
study
examines
effects
PMs
on
intercellular
adhesion
molecule-1
(ICAM-1)
expression
related
in
vitro
vivo.The
cytotoxicity,
reactive
oxygen
species
(ROS)
generation,
monocyte
adherence
A549
cells
were
more
severely
affected
by
treatment
O-PMs
(organic
solvent-extractable
fraction
SRM1649b)
than
W-PMs
(water-soluble
SRM1649b).
We
observed
a
significant
increase
ICAM-1
O-PMs,
but
not
W-PMs.
also
induced
phosphorylation
AKT,
p65,
STAT3.
Pretreating
N-acetyl
cysteine
(NAC),
an
antioxidant,
attenuated
O-PMs-induced
ROS
mentioned
kinases,
ICAM-1.
Furthermore,
AKT
inhibitor
(LY294002),
NF-κB
(BAY11-7082),
STAT3
(Stattic)
significantly
down-regulated
as
well
U937
epithelial
Interleukin-6
(IL-6)
was
most
changed
cytokine
O-PMs-treated
according
analysis
antibody
array.
The
IL-6
receptor
tocilizumab
(TCZ)
small
interfering
RNA
for
reduced
secretion
reduction
In
addition,
intratracheal
instillation
levels
tissues
plasma
WT
mice,
knockout
mice.
Pre-administration
NAC
those
PMs-induced
adverse
patients
chronic
obstructive
pulmonary
disease
(COPD)
had
higher
compared
healthy
subjects.These
results
suggest
vivo
through
IL-6/AKT/STAT3/NF-κB
signaling
pathway.
International Journal of Environmental Research and Public Health,
Journal Year:
2018,
Volume and Issue:
15(7), P. 1380 - 1380
Published: July 1, 2018
Air
pollution
is
a
very
critical
issue
worldwide,
particularly
in
developing
countries.
Particulate
matter
(PM)
type
of
air
that
comprises
heterogeneous
mixture
different
particle
sizes
and
chemical
compositions.
There
are
various
sources
fine
PM
(PM2.5),
the
components
may
also
have
effects
on
people.
The
pathogenesis
PM2.5
several
diseases
remains
to
be
clarified.
long
history
epidemiological
research
diseases.
Numerous
studies
show
can
induce
variety
chronic
diseases,
such
as
respiratory
system
damage,
cardiovascular
dysfunction,
diabetes
mellitus.
However,
evidence
associated
with
potential
mechanisms
progression
need
proved
precisely
through
vitro
vivo
investigations.
Suggested
lead
adverse
include
increasing
oxidative
stress,
inflammatory
responses,
genotoxicity.
aim
this
review
provide
brief
overview
experimental
from
last
decade.
summarized
results
could
clear
information
about
PM2.5-induced
disease.
Diabetes Care,
Journal Year:
2016,
Volume and Issue:
39(4), P. 547 - 554
Published: Feb. 11, 2016
OBJECTIVE
Recent
studies
suggest
that
air
pollution
plays
a
role
in
type
2
diabetes
(T2D)
incidence
and
mortality.
The
underlying
physiological
mechanisms
have
yet
to
be
established.
We
hypothesized
adversely
affects
insulin
sensitivity
secretion
serum
lipid
levels.
RESEARCH
DESIGN
AND
METHODS
Participants
were
selected
from
BetaGene
(n
=
1,023),
study
of
resistance
pancreatic
β-cell
function
Mexican
Americans.
All
participants
underwent
DXA
oral
intravenous
glucose
tolerance
tests
completed
dietary
physical
activity
questionnaires.
Ambient
pollutant
concentrations
(NO2,
O3,
PM2.5)
for
short-
long-term
periods
assigned
by
spatial
interpolation
(maximum
radius
50
km)
data
quality
monitors.
Traffic-related
freeways
(TRAP)
was
estimated
using
the
dispersion
model
as
NOx.
Variance
component
models
used
analyze
individual
multiple
associations
with
metabolic
traits.
RESULTS
Short-term
(up
58
days
cumulative
lagged
averages)
exposure
PM2.5
associated
lower
HDL-to-LDL
cholesterol
ratio
higher
fasting
insulin,
HOMA-IR,
total
cholesterol,
LDL
(LDL-C)
(all
P
≤
0.036).
Annual
average
glucose,
LDL-C
(P
0.043).
effects
short-term
on
largest
among
obese
participants.
No
statistically
significant
found
between
TRAP
outcomes.
CONCLUSIONS
Exposure
ambient
pollutants
tolerance,
sensitivity,
blood
concentrations.
Our
findings
may
contribute
pathophysiology
development
T2D
related
sequelae.
Free Radical Biology and Medicine,
Journal Year:
2017,
Volume and Issue:
110, P. 345 - 367
Published: June 29, 2017
Exposure
to
ambient
air
pollution
is
associated
with
adverse
cardiovascular
outcomes.
These
are
manifested
through
several,
likely
overlapping,
pathways
including
at
the
functional
level,
endothelial
dysfunction,
atherosclerosis,
pro-coagulation
and
alterations
in
autonomic
nervous
system
balance
blood
pressure.
At
numerous
points
within
each
of
these
pathways,
there
potential
for
cellular
oxidative
imbalances
occur.
The
current
review
examines
epidemiological,
occupational
controlled
exposure
studies
research
employing
healthy
diseased
animal
models,
isolated
organs
cell
cultures
assessing
importance
pro-oxidant
development
disease
collective
body
data
provides
evidence
that
stress
(OS)
not
only
central
eliciting
specific
cardiac
endpoints,
but
also
implicated
modulating
risk
succumbing
disease,
sensitivity
ischemia/reperfusion
injury
onset
progression
metabolic
following
exposure.
To
add
this
large
effort
conducted
date,
further
work
required
provide
greater
insight
into
areas
such
as
(a)
whether
an
imbalance
triggers
and/or
worsens
effect
representative
consequence
progression,
(b)
OS
outcomes
caused
by
individual
pollutants
mixtures,
or
a
inter-pollutant
interactions
(c)
protection
provided
nutritional
supplements
pharmacological
agents
antioxidant
properties,
susceptible
populations
residing
polluted
urban
cities.