Abstract:For
fish,
ammonia
toxicity
is
closely
related
to
ferroptosis,
oxidative
stress
and
inflammatory
responses.
Iron
an
essential
trace
element
that
plays
a
key
role
in
many
biological
processes
for
cells
organisms,
including
response
inflammation.
The
current
study
aimed
investigate
the
effect
of
iron
on
above
three
aspects
indicators
upon
exposure
fish.
head
kidney
macrophages
yellow
catfish
were
randomized
into
CON
group
(normal
control),
AM
(0.046
mg
L-1
total
nitrogen),
Fe
(20
µg
mL-1
FeSO4),
Fe+AM
FeSO4,
0.046
nitrogen).
Cells
pretreated
with
FeSO4
6
h
followed
by
24
h.
results
showed
supplementation
triggered
ferroptosis
(an
increase
level,
upregulation
transferrin
receptor
1)
(ROS
accumulation,
reduction
T-AOC,
downregulation
SOD,
CAT
Nrf2),
up-regulated
mRNA
expression
p53
anti-inflammatory
M2
macrophage
maker
(Arg-1),
promoted
progression
small
portion
from
early
apoptosis
late
apoptotic
cells.
But
combination
treatment
caused
stronger
intracellular
reaction
than
either
alone.
Meanwhile,
there
was
obvious
necrotic
groups.
findings
this
indicate
functions
fish
may
vary
inconsistently
presence
or
absence
stress.
Journal of Marine Science and Engineering,
Journal Year:
2024,
Volume and Issue:
12(6), P. 970 - 970
Published: June 8, 2024
This
study
aimed
to
explore
the
impact
of
acute
acidification
on
antioxidant,
metabolic
performance,
and
liver
histology
juvenile
yellowfin
tuna.
The
experiment
subjected
tuna
a
pH
gradient
environment
8.1,
7.6,
7.1,
6.6
for
48
h.
findings
indicate
that
seawater
7.1
significantly
impacts
antioxidant
systems
in
comparison
control
group.
At
there
were
observed
increases
glutathione
reductase
(GR),
total
capacity
(T-AOC),
lactate
dehydrogenase
(LDH),
hexokinase
(HK),
pyruvate
kinase
(PK),
sodium-potassium
ATPase
(Na+K+-ATP),
calcium-magnesium
(Ca2+Mg2+-ATP).
Conversely,
low-density
lipoprotein
cholesterol
(LDL-C),
high-density
(HDL-C),
triglycerides
(TGs)
not
different
across
treatment
groups.
However,
an
increase
transaminases
at
suggested
potential
damage,
which
was
further
supported
by
structural
tissue
degeneration
hepatocyte
vacuolation.
In
conclusion,
under
conditions
stress,
is
decrease
suppression
levels
tuna,
leading
oxidative
damage.
lays
foundation
in-depth
understanding
response
mechanisms
as
well
healthy
farming
broader
context
acidification.
Metabolites,
Journal Year:
2024,
Volume and Issue:
14(12), P. 649 - 649
Published: Nov. 21, 2024
Background:
Ammonia,
a
ubiquitous
contaminant
in
aquatic
ecosystems,
poses
multifaceted
threats
to
fish
species
at
elevated
concentrations.
Methods:
In
order
investigate
the
toxic
effects
of
chronic
ammonia
stress
on
liver
juvenile
Micropterus
salmoides,
present
experiment
was
conducted
differences
changes
tissue
structure,
enzyme
activities,
and
metabolomes
after
28
days
exposure
(0,
4,
8,
16
mg/L).
Results:
The
findings
revealed
that
induced
significant
oxidative
liver,
manifesting
decreased
activities
antioxidant
enzymes
SOD
GSH-Px,
levels
GSH,
GST,
MDA,
heightened
immune
LZM,
ALP,
ACP.
An
increase
concentration
exacerbated
damage.
Metabolome
analysis
further
unveiled
perturbations
metabolites
salmoides
exposed
ammonia,
with
Ala-His
emerging
as
potentially
pivotal
functional
substance
under
stress.
Specifically,
4
mg/L
group
responded
toxicity
by
augmenting
GSH
L-Carnosine
levels,
8
detoxified
via
upregulation
L-Glutamine,
mitigated
through
urea
synthesis
pathway.
Conclusions:
This
research
offers
preliminary
insights
into
toxicological
responses
It
is
suggested
duration
exceeding
high-density
aquaculture
should
not
exceed
7
days.
Abstract:For
fish,
ammonia
toxicity
is
closely
related
to
ferroptosis,
oxidative
stress
and
inflammatory
responses.
Iron
an
essential
trace
element
that
plays
a
key
role
in
many
biological
processes
for
cells
organisms,
including
response
inflammation.
The
current
study
aimed
investigate
the
effect
of
iron
on
above
three
aspects
indicators
upon
exposure
fish.
head
kidney
macrophages
yellow
catfish
were
randomized
into
CON
group
(normal
control),
AM
(0.046
mg
L-1
total
nitrogen),
Fe
(20
µg
mL-1
FeSO4),
Fe+AM
FeSO4,
0.046
nitrogen).
Cells
pretreated
with
FeSO4
6
h
followed
by
24
h.
results
showed
supplementation
triggered
ferroptosis
(an
increase
level,
upregulation
transferrin
receptor
1)
(ROS
accumulation,
reduction
T-AOC,
downregulation
SOD,
CAT
Nrf2),
up-regulated
mRNA
expression
p53
anti-inflammatory
M2
macrophage
maker
(Arg-1),
promoted
progression
small
portion
from
early
apoptosis
late
apoptotic
cells.
But
combination
treatment
caused
stronger
intracellular
reaction
than
either
alone.
Meanwhile,
there
was
obvious
necrotic
groups.
findings
this
indicate
functions
fish
may
vary
inconsistently
presence
or
absence
stress.