Journal of Applied Toxicology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Aug. 1, 2024
Given
its
antioxidant,
anti-inflammatory,
and
antiapoptotic
properties,
melatonin
(MEL),
a
health-caring
food
to
improve
sleep
disorders,
is
hypothesized
protect
against
nanomaterial
exposure-induced
toxicity.
However,
the
conclusion
derived
from
different
studies
seemed
inconsistent.
A
meta-analysis
of
all
available
preclinical
was
performed
examine
effects
MEL
on
nanomaterial-induced
damages.
Eighteen
relevant
were
retrieved
through
searching
five
electronic
databases
up
December
2023.
The
showed
that
relative
control,
treatment
significantly
increased
cell
viability
(standardized
mean
difference
[SMD
=
1.27])
alleviated
liver
function
(lowered
AST
-3.89]
ALT
-5.89]),
bone
formation
(enhanced
BV/TV
4.13]
lessened
eroded
surface
-5.40]),
brain
nerve
(inhibition
AChE
activity
-3.60])
damages
in
animals.
protective
mechanisms
caused
by
exposure
associated
with
(decreased
Bax/Bcl-2
ratio
-4.50]
caspase-3
levels
[dose
<100
μM:
SMD
-3.66]),
antioxidant
MDA
[in
vitro:
-2.84;
vivo:
-4.27]),
anti-inflammatory
(downregulated
TNF-α
-5.41;
-3.21]
IL-6
-5.90;
-2.81])
capabilities.
In
conclusion,
our
study
suggests
should
be
supplemented
prevent
populations
exposed
nanomaterials.
Frontiers in Human Neuroscience,
Journal Year:
2024,
Volume and Issue:
17
Published: Jan. 12, 2024
The
neuropathological
hallmarks
of
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
frontotemporal
lobar
degeneration
(FTLD),
and
amyotrophic
lateral
sclerosis
(ALS)
are
present
in
urban
children
exposed
to
fine
particulate
matter
(PM
2.5
),
combustion
friction
ultrafine
PM
(UFPM),
industrial
nanoparticles
(NPs).
Metropolitan
Mexico
City
(MMC)
forensic
autopsies
strongly
suggest
that
anthropogenic
UFPM
NPs
reach
the
brain
through
nasal/olfactory,
lung,
gastrointestinal
tract,
skin,
placental
barriers.
Diesel-heavy
unregulated
vehicles
a
key
source
for
21.8
million
MMC
residents.
We
found
hyperphosphorylated
tau,
beta
amyloid
1-42
,
α-synuclein,
TAR
DNA-binding
protein-43
were
associated
with
186
(mean
age
27.45
±
11.89
years).
neurovascular
unit
is
an
early
anatomical
target,
first
two
decades
life
critical:
100%
57
aged
14.8
5.2
years
had
AD
pathology;
25
(43.9%)
AD+TDP-43;
11
(19.3%)
+
PD
TDP-43;
2
(3.56%)
+PD.
Fe,
Ti,
Hg,
Ni,
Co,
Cu,
Zn,
Cd,
Al,
Mg,
Ag,
Ce,
La,
Pr,
W,
Ca,
Cl,
K,
Si,
S,
Na,
C
seen
frontal
temporal
lobes,
olfactory
bulb,
caudate,
substantia
nigra,
locus
coeruleus,
medulla,
cerebellum,
and/or
motor
cortical
spinal
regions.
Endothelial,
neuronal,
glial
damages
extensive,
mitochondria,
rough
endoplasmic
reticulum,
Golgi
apparatus,
lysosomes.
Autophagy,
cell
nuclear
membrane
damage,
disruption
pores
heterochromatin,
death
present.
Metals
abrasion
deterioration
automobile
catalysts
electronic
waste
rare
earth
elements,
i.e.,
lanthanum,
cerium,
praseodymium,
entering
young
brains.
Exposure
environmental
prime
candidates
initiating
stages
fatal
neurodegenerative
diseases.
adults—surrogates
polluted
areas
around
world—exhibit
AD,
PD,
FTLD,
ALS
forecasting
serious
health,
social,
economic,
academic,
judicial
societal
detrimental
impact.
Neurodegeneration
prevention
should
be
public
health
priority
as
problem
human
exposure
particle
pollution
solvable.
knowledgeable
main
emission
sources
technological
options
control
them.
What
we
waiting
for?
Environmental Toxicology and Pharmacology,
Journal Year:
2024,
Volume and Issue:
110, P. 104529 - 104529
Published: Aug. 9, 2024
Inhaled
particulate
matter
(PM)
is
a
key
factor
in
millions
of
yearly
air
pollution-related
deaths
worldwide.
The
oxidative
potential
PM
indicates
its
ability
to
promote
an
environment.
Excessive
reactive
oxygen
species
(ROS)
can
cause
cell
damage
via
stress,
leading
inflammation,
endoplasmic
reticulum
airway
remodeling,
and
various
death
modes
(apoptosis,
ferroptosis,
pyroptosis).
ROS
also
interact
with
macromolecules,
inducing
DNA
epigenetic
modifications,
disrupting
homeostasis.
These
effects
have
been
studied
extensively
vitro
confirmed
vivo.
This
review
explores
the
airborne
particles
PM-induced
ROS-mediated
cellular
observed
vitro,
highlighting
link
between
described
latest
literature.
analyzes
on
damage,
repair,
carcinogenicity,
epigenetics.
Additionally,
developments
antioxidants
prevent
ROS's
harmful
are
described,
providing
future
perspectives
topic.
Frontiers in Neuroscience,
Journal Year:
2023,
Volume and Issue:
17
Published: Aug. 4, 2023
To
prospectively
assess
whether
air
pollution,
including
PM2.5,
PM10,
and
NOx,
is
associated
with
the
risk
of
all-cause
dementia,
Alzheimer's
disease
(AD),
vascular
to
investigate
potential
relationship
between
pollution
genetic
susceptibility
in
development
AD.Our
study
included
437,932
participants
from
UK
Biobank
a
median
follow-up
period
over
10
years.
Using
Cox
proportional
hazards
model,
we
found
that
exposed
PM2.5
levels
≥10
μg/m3
had
higher
developing
dementia
(HR
=
1.1;
95%
CI:
1.05-1.28;
p
<
0.05)
compared
group
<10
μg/m3.
However,
there
was
no
significant
association
PM10
≥15
AD,
or
when
<15
On
other
hand,
NOx
≥50
significantly
1.14;
1.02-1.26;
AD
1.26;
1.08-1.48;
<50
Furthermore,
examined
combined
effect
(PM2.5,
NOx)
score
(AD-GRS)
on
using
model.
Among
high
AD-GRS,
those
1.36;
1.03-1.18;
0.05).
Regardless
pollutant
NOx),
AD-GRS
increased
AD.
Similar
results
were
obtained
assessing
multiple
variables
inverse
probability
treatment
weighting
(IPTW).Our
findings
indicate
individuals
living
areas
are
at
dementia.
Moreover,
demonstrated
an
particularly
presence
≥
50
Toxics,
Journal Year:
2025,
Volume and Issue:
13(4), P. 284 - 284
Published: April 8, 2025
Air
pollution
plays
a
key
role
in
sleep
disorders
and
neurodegeneration.
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
and/or
transactive
response
DNA-binding
protein
TDP-43
neuropathology
have
been
documented
children
young
adult
forensic
autopsies
the
metropolitan
area
of
Mexico
City
(MMC),
along
with
disorders,
cognitive
deficits,
MRI
brain
atrophy
seemingly
healthy
populations.
Ultrafine
particulate
matter
(UFPM)
industrial
nanoparticles
(NPs)
reach
urbanites’
brains
through
nasal/olfactory,
lung,
gastrointestinal
tract,
placental
barriers.
We
Fe
UFPM/NPs
neurovascular
units,
as
well
lateral
hypothalamic
nucleus
orexinergic
neurons,
thalamus,
medullary,
pontine,
mesencephalic
reticular
formation,
pinealocytes.
quantified
ferromagnetic
materials
arousal
hubs
examined
their
motion
behavior
to
low
magnetic
fields
MMC
autopsy
samples
from
nine
25
adults
AD,
PD,
neuropathology.
Saturated
isothermal
remanent
magnetization
curves
at
50–300
mT
were
associated
UFPM/NP
accumulation
sleep/awake
30–50
µT
(DC
fields)
exposure.
Brain
exposed
anthropogenic
PM
found
be
sensitive
fields,
behaviors
that
potentially
linked
early
development
progression
fatal
neurodegenerative
diseases
disorders.
Single-domain
orexin
system,
arousal,
sleep,
autonomic
regions,
are
neurodegeneration,
behavioral
impairment,
need
identify
higher
risk
monitor
environmental
UFPM
NP
emissions
exposures
fields.
Ubiquitous
ferrimagnetic
particles
field
threat
global
health.
Brain Sciences,
Journal Year:
2025,
Volume and Issue:
15(5), P. 498 - 498
Published: May 13, 2025
Amyotrophic
lateral
sclerosis
(ALS/MND)
is
considered
a
uniquely
human
complex
neurodegenerative
disorder,
presenting
with
variety
of
clinical
phenotypes,
which
include
frontotemporal
dementia
[...].