TY - JOUR
T1 - Nadolol inhibits reactive oxygen species generation by leukocytes and linoleic acid oxidation
AU - Magsino, Cesar H.
AU - Hamouda, Wael
AU - Bapna, Vini
AU - Ghanim, Husam
AU - Abu-Reish, Ihab A.
AU - Aljada, Ahmad
AU - Dandona, Paresh
N1 - Funding Information:
This study was supported in part by the Wm McGowan Charitable Fund, Inc.
PY - 2000/8/15
Y1 - 2000/8/15
N2 - We studied the effect of short-term nadolol administration on the reactive oxygen species (ROS) generation by polymorphonuclear leukocytes and mononuclear cells in 8 normal subjects. At a oral dose of 40 mg/day for 5 days, nadolol produced a decrease in the ROS generation by leukocytes. ROS generation by polymorphonuclear leukocytes decreased by 38% from 134 ± 44 mV at baseline to 83 ± 34 mV after 5 days (p = 0.005), and ROS generation by mononuclear cells decreased by 33% from 174 ± 69 mV at baseline to 117 ± 55 mV after 5 days (p = 0.015). There was also a significant reduction in linoleic acid oxidation as reflected by the lower levels of 9- and 13- hydroxy-octadecadienoic acid after 5 days. There was no change in the plasma thiobarbituric acid-reacting substances, a less sensitive index of oxidative damage to lipids. There was also no significant change in the levels of metatyrosine and orthotyrosine, which are known indexes of oxidative damage to amino acids and proteins. The absence of a significant change in metatyrosine, orthotyrosine, and thiobarbituric acid-reacting substances may reflect the short duration of nadolol administration and the decreased ROS load. Because ROS may induce lipid peroxidation, this inhibitory effect of nadolol on ROS generation by leukocytes and linoleic acid oxidation may inhibit low-density lipoprotein oxidation and thus atherogenesis. This effect may partly explain the favorable outcomes observed in patients with coronary artery disease on long-term β-blocker therapy.
AB - We studied the effect of short-term nadolol administration on the reactive oxygen species (ROS) generation by polymorphonuclear leukocytes and mononuclear cells in 8 normal subjects. At a oral dose of 40 mg/day for 5 days, nadolol produced a decrease in the ROS generation by leukocytes. ROS generation by polymorphonuclear leukocytes decreased by 38% from 134 ± 44 mV at baseline to 83 ± 34 mV after 5 days (p = 0.005), and ROS generation by mononuclear cells decreased by 33% from 174 ± 69 mV at baseline to 117 ± 55 mV after 5 days (p = 0.015). There was also a significant reduction in linoleic acid oxidation as reflected by the lower levels of 9- and 13- hydroxy-octadecadienoic acid after 5 days. There was no change in the plasma thiobarbituric acid-reacting substances, a less sensitive index of oxidative damage to lipids. There was also no significant change in the levels of metatyrosine and orthotyrosine, which are known indexes of oxidative damage to amino acids and proteins. The absence of a significant change in metatyrosine, orthotyrosine, and thiobarbituric acid-reacting substances may reflect the short duration of nadolol administration and the decreased ROS load. Because ROS may induce lipid peroxidation, this inhibitory effect of nadolol on ROS generation by leukocytes and linoleic acid oxidation may inhibit low-density lipoprotein oxidation and thus atherogenesis. This effect may partly explain the favorable outcomes observed in patients with coronary artery disease on long-term β-blocker therapy.
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U2 - 10.1016/S0002-9149(00)00962-0
DO - 10.1016/S0002-9149(00)00962-0
M3 - Article
C2 - 10946040
AN - SCOPUS:0342656103
SN - 0002-9149
VL - 86
SP - 443
EP - 448
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 4
ER -