Scientific Conference on Atherosclerosis, Thrombosis, and Proliferation, American Heart Association, Orlando, FL, February 23-26, 1994.
Hari M. Sharma, Atef N. Hanna, Lynda C. Titterington, Gary P. Lubow, and Ralph E. Stephens.
The Ohio State University, Columbus, OH
MAK-4 and MAK-5 inhibit Cu+2-catalyzed LDL oxidation and liver microsomal lipid peroxidation. In this study, we examined the ability of antioxidants to inhibit endothelial cell (EC)- and Soybean lipoxygenase (SLP)-induced LDL oxidation, and total antioxidant capacity to absorb peroxyl free radicals. Both aqueous and alcoholic extracts of MAK-4 and MAK-5 inhibited the EC-induced LDL oxidation in a concentration-dependent manner. The concentrations (ug/2mL) that produce 50% inhibition (IC50) for aqueous extracts of MAK-4 and MAK-5 were 100.4 ± 6.2, 180.6 ± 17.9, and alcoholic extracts of MAK-4 and MAK-5, 57.5 ± 15.2, 7.10 ± 2.26, respectively, for TBARS. MAK-4 and MAK-5 caused prolongation of the lag phase and delay of the propagation phase of EC-LDL oxidation. Both aqueous and alcoholic extracts of MAK-4 inhibited the SLP-induced LDL oxidation in a concentration-dependent manner [IC50 were 840.6 ± 196.6 and 246.4 ± 32.5, respectively]. The aqueous extract of MAK-5 inhibited SLP-induced LDL oxidation in a concentration-dependent manner [IC50 was 503.0 ± 139.4] and Vit. C inhibited up to 35% at a concentration of 200 uM, whereas estradiol and estrone were ineffective up to 20 uM. Vit. C, MAK-4 and MAK-5 showed a concentration-dependent potency in absorbing peroxyl radicals. These results suggest that MAK-4 and MAK-5 possess antioxidant activity and might be beneficial in atherosclerosis.
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