Biomolecules,
Journal Year:
2020,
Volume and Issue:
10(12), P. 1702 - 1702
Published: Dec. 21, 2020
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
often
the
hepatic
expression
of
metabolic
syndrome
and
its
comorbidities
that
comprise,
among
others,
obesity
insulin-resistance.
NAFLD
involves
a
large
spectrum
clinical
conditions.
These
range
from
steatosis,
benign
disorder
characterized
by
accumulation
fat
in
hepatocytes,
to
non-alcoholic
steatohepatitis
(NASH),
which
inflammation,
hepatocyte
damage,
fibrosis.
NASH
can
further
progress
cirrhosis
hepatocellular
carcinoma.
The
etiology
both
genetic
environmental
factors,
including
an
unhealthy
lifestyle.
Of
note,
eating
clearly
associated
with
development
progression
NASH.
Both
macronutrients
(sugars,
lipids,
proteins)
micronutrients
(vitamins,
phytoingredients,
antioxidants)
affect
pathogenesis.
Furthermore,
some
evidence
indicates
disruption
homeostasis
food
contaminants,
are
risk
factor
candidates
NAFLD.
At
molecular
level,
several
models
have
been
proposed
for
pathogenesis
Most
importantly,
oxidative
stress
mitochondrial
damage
reported
be
causative
initiation
progression.
aim
this
review
provide
overview
contribution
nutrients
especially
pesticides,
how
they
may
influence
Environment International,
Journal Year:
2019,
Volume and Issue:
135, P. 105399 - 105399
Published: Dec. 23, 2019
Neonicotinoid
insecticides
are
ubiquitous
in
food
and
the
environment
due
to
their
wide
use.
Growing
evidence
suggests
adverse
effects
of
neonicotinoids
many
species,
including
mammals.
Some
studies
have
reported
urinary
concentrations
human
biological
monitoring,
but
potential
risks
on
health
based
long-term
chronic
exposure
any
general
population
been
rarely
tackled.
In
this
study,
dietary
Chinese
adult
was
studied
basis
composite
samples
collected
from
5th
(2009–2012)
6th
(2015–2018)
total
diet
(TDS).
Residue
levels
ten
were
determined
528
24
provinces
China.
Most
(53.3%
70.5%
TDS,
respectively)
that
we
analyzed
contained
multi-residue
neonicotinoids.
Imidacloprid
acetamiprid
most
frequently
detected
neonicotinoids,
thiamethoxam
clothianidin
increasingly
used
found
TDS.
The
estimated
daily
intake
(EDI)
for
calculated
evaluate
risk
a
relative
potency
factor
assessment
method.
mean
EDIs
TDS
respectively
reached
598.95
710.38
ng/kg
bw
per
day.
Although
neonics
relatively
higher
than
no
statistical
difference
observed
(p
>
0.05).
Vegetables
main
source
exposure,
via
cereals
beverages
water
must
also
be
addressed
average
much
lower
current
reference
dose
(57
μg/kg
day),
should
not
overlooked
ubiquity
environment.
The Science of The Total Environment,
Journal Year:
2019,
Volume and Issue:
700, P. 134914 - 134914
Published: Oct. 28, 2019
In
the
present
work,
marine
invertebrate
Mytilus
galloprovincialis
was
used
as
model
organism
to
evaluate
toxic
effects
of
neonicotinoid
Calypso
480
SC
(CAL)
following
20
days
exposure
sub-lethal
concentrations
7.77
mg
L-1
(0.1%
96
h-LC50)
and
77.70
(1%
h-LC50),
a
recovery
period
10
in
uncontaminated
seawater.
Results
revealed
that
both
CAL
increased
significantly
mortality
rate
cells
haemolymph
digestive
gland,
while
gland
were
no
longer
able
regulate
cell
volume.
Exposure
reduced
parameters
(Cl-,
Na+),
affected
enzymatic
activities
superoxide
dismutase
catalase
gill,
caused
also
histopathological
alterations
gills.
Main
histological
damages
detected
mussels
lipofuscin
accumulation,
focal
points
necrosis,
mucous
overproduction
infiltrative
inflammations.
Interestingly,
persisted
after
CAL-free
water,
especially
for
haemocyte
(K+,
Na+,
Ca2+,
lactate
dehydrogenase,
glucose).
A
slight
conditions
detected.
These
findings
suggested
sub-chronic
insecticide
significant
tissue
M.
galloprovincialis.
Considering
ecologically
commercially
important
role
coastal
waters,
potential
risk
posed
by
neonicotinoids
this
essential
aquatic
resource
can
be
highlighted.
Biomolecules,
Journal Year:
2020,
Volume and Issue:
10(12), P. 1702 - 1702
Published: Dec. 21, 2020
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
often
the
hepatic
expression
of
metabolic
syndrome
and
its
comorbidities
that
comprise,
among
others,
obesity
insulin-resistance.
NAFLD
involves
a
large
spectrum
clinical
conditions.
These
range
from
steatosis,
benign
disorder
characterized
by
accumulation
fat
in
hepatocytes,
to
non-alcoholic
steatohepatitis
(NASH),
which
inflammation,
hepatocyte
damage,
fibrosis.
NASH
can
further
progress
cirrhosis
hepatocellular
carcinoma.
The
etiology
both
genetic
environmental
factors,
including
an
unhealthy
lifestyle.
Of
note,
eating
clearly
associated
with
development
progression
NASH.
Both
macronutrients
(sugars,
lipids,
proteins)
micronutrients
(vitamins,
phytoingredients,
antioxidants)
affect
pathogenesis.
Furthermore,
some
evidence
indicates
disruption
homeostasis
food
contaminants,
are
risk
factor
candidates
NAFLD.
At
molecular
level,
several
models
have
been
proposed
for
pathogenesis
Most
importantly,
oxidative
stress
mitochondrial
damage
reported
be
causative
initiation
progression.
aim
this
review
provide
overview
contribution
nutrients
especially
pesticides,
how
they
may
influence
