The
creation
of
mitochondria-targeted
vector
systems
is
a
new
tool
for
the
treatment
socially
significant
diseases.
Phosphonium
groups
provide
targeted
delivery
drugs
through
biological
barriers
to
organelles.
For
this
purpose,
class
alkyl(diethylamino)(phenyl)
phosphonium
iodides
(bromides)
1
containing
one,
two,
or
three
diethylamino
were
obtained
by
reaction
alkyl
with
(diethylamino)(phenyl)phosphines
under
mild
conditions
and
high
yields.
structure
compounds
was
established
NMR
XRD.
In
vitro
cytotoxicity
against
lines
M-Hela,
HuTu
80,
PC3,
DU-145,
PANC-1
MCF-7
found.
Selectivity
index
are
in
range
0.06-4.0
M
(SI
17-277)
most
active
compounds.
ROS
production,
mitochondrial
localization
process
cellular
apoptosis
investigated.
Decorated
lipid
(liposomes
solid
nanoparticles)
improve
decrease
toxicity
normal
cell
lines.
Compounds
induce
proceeding
along
pathway.
Aminophosphonium
salts
also
exhibit
selective
activity
Gram-positive
bacteria
strains
S.
aureus
209P,
B.
segeus
8035,
including
methicillin-resistant
(MRSA-1,
MRSA-2),
comparable
fluoroquinolone
antibiotic
norfloxacin.
A
moderate
vivo
CD-1
mice
lead
ABSTRACT
Background
In
recent
decades,
natural
compounds
have
been
considered
a
significant
source
of
new
antitumor
medicines
due
to
their
unique
advantages.
Several
in
vitro
and
vivo
studies
focused
on
the
effect
terpenoids
apoptosis
mediated
by
mitochondria
malignant
cells.
Recent
findings
this
review
article,
we
six
extensively
studied
terpenoids,
including
sesquiterpenes
(dihydroartemisinin
parthenolide),
diterpenes
(oridonin
triptolide),
triterpenes
(betulinic
acid
oleanolic
acid),
efficacy
targeting
induce
cell
death.
Terpenoid‐induced
mitochondria‐related
death
includes
apoptosis,
pyroptosis,
necroptosis,
ferroptosis,
autophagy,
necrosis
caused
mitochondrial
permeability
transition.
Apoptosis
autophagy
interact
meaningful
ways.
addition,
view
several
disadvantages
such
as
low
stability
bioavailability,
advances
research
combination
chemotherapy
chemical
modification
were
surveyed.
Conclusion
This
article
deepens
our
understanding
association
between
death,
presenting
hypothetical
basis
for
use
anticancer
management.
Toxicology and Industrial Health,
Год журнала:
2024,
Номер
unknown
Опубликована: Сен. 17, 2024
Nanoparticles
(NPs)
are
utilized
in
various
applications,
posing
potential
risks
to
human
health,
tissues,
cells,
and
macromolecules.
This
study
aimed
investigate
the
ultrastructural
alterations
hepatocytes
renal
tubular
cells
induced
by
metallic
metal
oxide
NPs.
Adult
healthy
male
Wistar
albino
rats
(
Rattus
norvegicus)
were
divided
into
6
n
=
7)
control
treated
groups
7).
The
exposed
daily
silver
NPs,
gold
zinc
silicon
dioxide
copper
ferric
NPs
for
35
days.
members
of
group
each
corresponding
received
respective
vehicle.
Liver
kidney
tissue
blocks
from
all
processed
Transmission
Electron
Microscopy
(TEM)
examinations.
NPs-treated
demonstrated
mitochondrial
mainly
cristolysis,
swelling,
membrane
disruption,
lucent
matrices,
matrices
lysis,
electron-dense
deposits.
However,
other
organelles
injury
but
a
lesser
extent
form
shrunken
nuclei,
nuclear
indentation,
endoplasmic
reticulum
fragmentation,
cellular
membranes
enfolding,
brush
border
microvilli
lysosomal
hyperplasia,
ribosomes
dropping,
peroxisome
formation.
One
may
conclude
findings
that
mitochondria
main
targets
nanoparticles
toxicity
ending
disruption
cell
injury.
Further
studies
taking
account
relation
damage
with
weakened
antioxidant
defense
system
chronic
exposure
nanomaterials
needed.
The
coronavirus
disease
2019
(COVID-19),
caused
by
severe
acute
respiratory
syndrome
2
(SARS-CoV-2),
has
presented
global
challenges
with
a
diverse
clinical
spectrum,
including
complications
and
systemic
effects.
This
review
explores
the
intricate
relationship
between
mitochondrial
dysfunction,
aging,
obesity
in
COVID-19.
Mitochondria
are
vital
for
cellular
energy
provision
resilience
against
age-related
macromolecule
damage
accumulation.
They
manage
allocation
cells,
activating
adaptive
responses
stress
signals
such
as
redox
imbalance
innate
immunity
activation.
As
organisms
age,
function
diminishes.
Aging
obesity,
linked
to
compromise
antiviral
response,
affecting
release
of
interferons,
worsening
COVID-19
severity.
Furthermore,
development
post-acute
sequelae
SARS-CoV-2
infection
(PASC),
also
known
long
COVID
been
associated
altered
metabolism,
chronic
immune
dysregulation
derived
from
dysfunction.
Understanding
interplay
mitochondria,
viral
infections
provides
insights
into
pathogenesis.
Targeting
health
may
offer
potential
therapeutic
strategies
mitigate
outcomes
address
long-term
consequences
infected
individuals.
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Апрель 13, 2024
Abstract
Mitochondrial
dynamics
are
emerging
as
master
regulators
for
targeting
several
types
of
cancers,
including
breast
cancer,
cervical
and
hepatocellular
carcinoma,
therapeutic
intervention.
morphology,
size,
position
activity
within
cells
is
regulated
by
dynamic
fission
fusion
events.
Dynamin-related
protein
1
(
Drp1
)
promotes
mitochondrial
maintains
homeostasis.
Loss
Scrib
implicated
in
human
cancers
wherein
dysfunction
leads
to
excessive
cell
proliferation
metastasis.
However,
the
exact
molecular
mechanisms
behind
loss
induced
dysregulation
cancer
progression
remains
obscure.
Although
role
being
investigated
but
-
mediated
event
regulating
maintenance
polarity
upon
function
elusive.
In
this
study,
first
time,
we
blocked
knockdown
metastasis
model
two
ways,
firstly,
through
genetic
ablation
Drp1,
secondly
using
mdivi-1,
a
specific
inhibitor.
Genetic
depletion
expression
RNAi
inhibits
Metalloproteinase
MMP1
,
reduces
ROS
production,
restores
apico-basal
(A/B)
enhances
ATP
production.
Further
confirm
regulation
polarity,
employed
mdivi,
inhibitor
which
has
dose
dependent
effect
regulation.
This
study
also
reveals
that
JNK
inhibition
abrogated
mitigates
controls
leading
restoration
morphology
epithelial
cellpolarity.
Our
results
highlight
key
regulator
maintaining
gets
affected
Drp1-JNK
downregulation
effectively
associated
proliferation,
pupal
lethality
phenotypes.
AJP Cell Physiology,
Год журнала:
2024,
Номер
327(2), С. C254 - C269
Опубликована: Май 27, 2024
The
podocyte
cytoskeleton
determines
the
stability
of
structure
and
function,
their
imbalance
plays
a
pathogenic
role
in
diseases.
However,
underlying
mechanism
damage
is
not
fully
understood.
Here,
we
investigate
specific
cuproptosis
inducing
injury.
In
vitro
vivo
studies,
exposure
to
high
levels
copper
adriamycin
(ADR)
caused
significant
increases
concentration
intracellular
renal
tissue.
Moreover,
excessive
accumulation
induced
cuproptosis,
resulting
destruction
cytoskeleton.
inhibition
reduce
also
significantly
alleviated
addition,
mitigated
ADR-induced
mitochondrial
as
well
production
reactive
oxygen
species
depolarization
membrane
potential,
restored
adenosine
triphosphate
(ATP)
synthesis.
Among
transcriptome
sequencing
data,
difference
CXCL5
(C-X-C
motif
chemokine
ligand
5)
was
most
significant.
Both
ADR
can
cause
upregulation
CXCL5,
deletion
inhibits
occurrence
thereby
alleviating
damage.
This
suggests
that
may
act
upstream
mediates
conclusion,
by
induce
promoting
dysfunction,
causing
indicates
an
important
pathogenesis
injury
provides
basis
for
seeking
potential
targets
treatment
chronic
kidney
disease.
Diagnostics,
Год журнала:
2024,
Номер
14(23), С. 2649 - 2649
Опубликована: Ноя. 24, 2024
This
is
a
structured
scoping
review
to
assess
whether
there
relationship
between
stress-induced
hyperglycemia
(SIH),
cytokine
interactions,
and
mortality
in
trauma
patients
comparison
non-diabetic
normoglycemia
[NDN],
diabetic
[DN],
[DH].
