Nanomaterials,
Journal Year:
2025,
Volume and Issue:
15(6), P. 441 - 441
Published: March 14, 2025
A
stabilized
biochar
(BC)–nano-scale
zero-valent
iron
(nZVI)
composite
(BC-nZVI@Cell-g-PAA)
was
prepared
using
cellulose-grafted
polyacrylic
acid
(Cell-g-PAA)
as
the
raw
material
through
in
situ
polymerization
and
liquid-phase
reduction
methods
for
remediation
of
hexavalent
chromium
(Cr(VI))-contaminated
water.
BC-nZVI@Cell-g-PAA
characterized
by
XRD,
FT-IR,
SEM,
BET,
TEM,
XPS.
According
to
batch
experiments,
under
optimized
conditions
(Cr(VI)
concentration
50
mg/L,
pH
=
3,
dosage
2
g/L),
achieved
maximum
Cr(VI)
removal
efficiency
(99.69%)
within
120
min.
Notably,
BC,
a
carrier,
high
dispersion
nZVI
its
porous
structure,
effectively
preventing
particle
agglomeration
improving
reaction
activity.
Simultaneously,
functional
groups
on
surface
Cell-g-PAA
provided
excellent
protection
nZVI,
significantly
suppressing
oxidative
deactivation.
Furthermore,
reduced
insoluble
trivalent
chromium(Cr(III))
species
them
immobilization.
The
synergistic
effects
physical
adsorption
chemical
greatly
contributed
Cr(VI).
Remarkably,
exhibited
reusability
with
62.4%
after
five
cycles,
demonstrating
potential
promising
remediating
Cr(VI)-contaminated
In
conclusion,
not
only
demonstrated
remarkable
but
also
showcased
practical
applications
environmental
remediation,
evidenced
sustained
performance
over
multiple
reuse
cycles.
Moreover,
Cr(VI),
toxic
carcinogenic
substance,
poses
significant
risks
aquatic
ecosystems
human
health,
underscoring
importance
developing
effective
from
contaminated
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(20), P. 12213 - 12213
Published: Oct. 13, 2022
Experimental
liver
injury
with
hepatocelluar
necrosis
and
abnormal
tests
is
caused
by
exposure
to
heavy
metals
(HMs)
like
aluminum,
arsenic,
beryllium,
cadmium,
chromium,
cobalt,
copper,
iron,
lead,
mercury,
molybdenum,
nickel,
platinum,
thallium,
titanium,
vanadium,
zinc.
As
pollutants,
HMs
disturb
the
ecosystem,
as
these
substances
are
toxic,
they
may
affect
health
of
humans
animals.
not
biodegradable
be
deposited
preferentially
in
liver.
The
use
animal
models
can
help
identify
molecular
mechanistic
steps
leading
injury.
commonly
initiate
hepatocellular
overproduction
ROS
(reactive
oxygen
species)
due
oxidative
stress,
resulting
covalent
binding
radicals
macromolecular
proteins
or
lipids
existing
membranes
subcellular
organelles.
Liver
facilitated
iron
via
Fenton
reaction,
providing
ROS,
triggered
if
protective
antioxidant
systems
exhausted.
Ferroptosis
syn
pyroptosis
was
recently
introduced
concept
explanations
nickel
(Ni)
NiCl2
causes
increased
deposition
liver,
upregulation
cyclooxygenase
2
(COX-2)
protein
mRNA
expression
levels,
downregulation
glutathione
eroxidase
4
(GPX4),
ferritin
chain
1
(FTH1),
nuclear
receptor
coactivator
(NCOA4)
protein,
levels.
Nickel
cause
hepatic
through
mitochondrial
damage
ferroptosis,
defined
mechanism
iron-dependent
cell
death,
similar
glutamate-induced
excitotoxicity
but
likely
distinct
from
apoptosis,
necrosis,
autophagy.
Under
discussion
were
additional
concepts
uptake
biliary
excretion
mercury
exposed
For
instance,
organic
anion
transporter
3
(Oat3)
multidrug
resistance-associated
(Mrp2)
involved
handling
mercury.
Mercury
treatment
modified
Mrp2
Oat3
assessed
immunoblotting,
partially
explaining
its
impaired
excretion.
Concomitantly,
a
decrease
abundance
hepatocyte
plasma
observed
that
limits
ions.
Most
importantly
shown
for
first
time
HMs,
titanium
changed
diversity
gut
microbiota
their
metabolic
functions,
generation
lipopolysaccharides
(LPS).
endotoxins,
LPS
trigger
perpetuate
at
level
gut-liver.
In
sum,
experimental
HM
administration
complex,
key
promotional
compound.
However,
such
used
modification
systems,
endotoxins
derived
intestinal
bacteria
gut-liver
merit
further
consideration.
Journal of Advanced Research,
Journal Year:
2022,
Volume and Issue:
46, P. 87 - 100
Published: May 2, 2022
Lead
(Pb)
is
an
environmental
toxicant
that
poses
severe
health
risks
to
humans
and
animals,
especially
renal
disorders.
Pb-induced
nephrotoxicity
has
been
attributed
oxidative
stress,
in
which
apoptosis
autophagy
are
core
events.
Nuclear
factor
erythroid
2-related
2
(Nrf2)
acts
as
a
major
contributor
counteract
damage,
while
hyperactivation
or
depletion
of
Nrf2
pathway
can
cause
the
redox
imbalance
induce
tissue
injury.
This
study
was
performed
clarify
function
mechanism
Pb-triggered
kidney
First,
data
showed
Pb
exposure
activates
primary
rat
proximal
tubular
cells.
Next,
activation
effectively
regulated
by
pharmacological
modulation
siRNA-mediated
knockdown
vitro
vivo
assays.
Notably,
cytotoxicity,
injury
concomitant
were
improved
downregulation,
confirming
persistent
contributes
nephrotoxicity.
Additionally,
blockage
relieved
downregulation.
Mechanistically,
we
found
reduced
ubiquitination
nuclear-cytoplasmic
loss
Keap1
p62-dependent
manner.
In
conclusion,
these
findings
highlight
dark
side
potential
crosstalk
among
activation,
Journal of Advanced Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Jan. 1, 2024
Arsenic
has
been
ranked
as
the
most
hazardous
substance
by
U.S.
Agency
for
Toxic
Substances
and
Disease
Registry.
Environmental
arsenic
exposure-evoked
health
risks
have
become
a
vital
public
concern
worldwide
owing
to
widespread
existence
of
arsenic.
Multi-omics
is
revolutionary
technique
data
analysis
providing
an
integrated
view
bioinformation
comprehensively
systematically
understanding
elaborate
mechanism
diseases.
This
study
aimed
at
uncovering
potential
contribution
liver-microbiota-gut
axis
in
chronic
inorganic
exposure-triggered
biotoxicity
chickens
based
on
multi-omics
technologies.
Forty
Hy-Line
W-80
laying
hens
were
chronically
exposed
sodium
arsenite
with
dose-dependent
manner
(administered
drinking
water
containing
10,
20,
or
30
mg/L
arsenic,
respectively)
42
d,
followed
transcriptomics,
serum
non-targeted
metabolome,
16S
ribosomal
RNA
gene
sequencing
accordingly.
intervention
induced
serious
chicken
liver
dysfunction,
especially
severe
fibrosis,
simultaneously
altered
ileal
microbiota
populations,
impaired
intestinal
barrier,
further
drove
enterogenous
lipopolysaccharides
translocation
via
portal
vein
circulation
aggravating
damage.
Furtherly,
injured
disturbed
bile
acids
(BAs)
homoeostasis
through
strongly
up-regulating
BAs
synthesis
key
rate-limiting
enzyme
CYP7A1,
inducing
excessive
total
accumulation,
accompanied
massive
primary
BA—chenodeoxycholic
acid.
Moreover,
concentrations
secondary
BAs—ursodeoxycholic
acid
lithocholic
markedly
repressed,
which
might
involve
repressed
dehydroxylation
Ruminococcaceae
Lachnospiraceae
families.
Abnormal
metabolism
turn
promoted
injury,
ultimately
perpetuating
pernicious
circle
chickens.
Notably,
obvious
depletion
abundance
four
profitable
microbiota,
Christensenellaceae,
Ruminococcaceae,
Muribaculaceae,
Faecalibacterium,
correlated
tightly
this
hepato-intestinal
process
Our
demonstrates
that
exposure
evokes
disruption
establishes
scientific
basis
evaluating
risk
environmental
pollutant
