Page 108 - 79_04

Alexia
Gómez
&
col.

Table
5.-­-
Estimation
of
desaturase
activities
of
heart
mitochondria
from
control
or
atenolol
treated

Wistar
rats.

DESATURASES
Control
Atenolol

?9
(n-­-7)
C16:1/C16:0
0.046±0.001
0.048±0.002

?9
(n-­-9)
C18:1/C18:0
0.561±0.010
0.604±0.013*

?8
(n-­-6)
C20:3/C20:2
0.828±0.044
0.846±0.025

?5
(n-­-6)
C20:4/C20:3
15.387±0.795
12.123±0.493**

n-­-6*
C22:5/C18:2
0.099±0.009
0.058±0.004**

n-­-3*
C22:6/C18:3
14.289±1.494
9.141±0.566**

*
Integrated
desaturase/elongase
activities
for
the
n-­-6
and
n-­-3
series.

Table
6.-­-
Estimation
of
elongase
activities
of
heart
mitochondria
from
control
or
atenolol
treated

Wistar
rats.

ELONGASES
Control
Atenolol

ELOVL
3
(n-­-9)
C20:1/C18:1
0.019±0.003
0.015±0.001

ELOVL
6
C18:0/C16:0
1.033±0.029
0.991±0.023

ELOVL
1/3
C20:0/C18:0
0.007±0.001
0.007±0.001

ELOVL
1/3
C22:0/C20:0
1.371±0.048
1.018±0.051***

ELOVL
1/3
C24:0/C22:0
1.392±0.096
1.077±0.036**

ELOVL
5
(n-­-6)
C20:2/C18:2
0.086±0.004
0.065±0.003**

ELOVL
2/5
(n-­-6)
C22:4/C20:4
0.028±0.001
0.023±0.001*

ELOVL
2/5
(n-­-3)
C22:5/C20:5
7.508±0.418
6.071±0.443*

4.
DISCUSSION

In
the
present
investigation
the
effect
of
the
selective
ß-­-1
blocker
atenolol

on
oxidative
stress
related
parameters
was
studied
in
the
Wistar
rat
heart
for
the

first
time.
This
drug,
which
has
been
used
in
humans
for
decades
without
known

important
side
effects,
and
with
beneficial
effects
like
reduced
mortality
and

morbidity
reported
in
many
clinical
studies
(37),
decreased
the
fatty
acid

unsaturation
degree,
protein
lipoxidation
levels
and
desaturase
activities
after
two

weeks
of
treatment.
The
reported
decrease
in
fatty
acid
unsaturation
and
oxidative

stress
after
interruption
of
ß-­-adrenergic
receptor
signalling
induced
by
atenolol

could
be
one
of
the
mechanisms,
among
other,
responsible
for
the
longevity

increase
observed
in
129/SvJ-­-C57BL/6
AC5KO
mice
(1).
Atenolol
decreased
the

heart
fatty
acid
unsaturation
degree
of
atenolol-­-treated
C57BL/6
mice,
reducing

DBI,
PI
and
total
PUFA.
Atenolol
treatment
was
able
to
lower
protein
oxidation
and

lipoxidation
and
to
increase
p-­-ERK
levels
in
those
mice
too
(38).
In
the
present

investigation
we
wanted
to
clarify
if
atenolol
has
the
same
effects
in
genetically

624