An. Real. Acad. Farm. vol 79 nº 4 2013 - page 109

Alexia Gómez & col.
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Table 5.-­‐
Estimation of desaturase activities of heart mitochondria from control or atenolol treated
Wistar rats.
DESATURASES
Control
Atenolol
Δ9 (n-­‐7)
C16:1/C16:0
0.046±0.001
0.048±0.002
Δ9 (n-­‐9)
C18:1/C18:0
0.561±0.010
0.604±0.013*
Δ8 (n-­‐6)
C20:3/C20:2
0.828±0.044
0.846±0.025
Δ5 (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 β-­‐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 β-­‐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
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