The inhibition of LDL-oxidation by 17-alpha estradiol was assessed in vitro
by the determination of the duration of the lag-phase in copper ion-induce
d oxidation and compared to that of 17-beta estradiol, estriol, and probuco
l. Addition of 0.2, 0.4, and 1 mu mol/l of the test substances prolonged th
e lag-phase of LDL-oxidation 1.3-(+/-0.09 SD), 1.7-(+/-0.14 SD), and 2.7-(/-0.25 SD) fold for 17-alpha estradiol; 1.4-(+/-0.14 SD), 1.8-(+/-0.1 SD),
and 2.6-(+/-0.16 SD) fold for 17-beta estradiol; 1.1-(+/-0.07 SD), 1.4-(+/-
0.11 SD), and 1.6-(+/-0.11 SD) fold for estriol as well as 1.4-(+/-0.14 SD)
, 1.6-(+/-0.1 SD), and 3.0-(+/-0.21) fold for probucol, thus proving that 1
7-alpha estradiol is as effective as 17-beta estradiol or similar to probuc
ol and more effective than estriol (n = 6 in all cases). These data demonst
rate that 17-alpha estradiol is able to delay LDL-oxidation, hence providin
g a basis for clinical examination of the protective effects of 17-alpha es
tradiol against artherosclerosis in patients where hormonal effects of 17-b
eta estradiol are undesirable.