title: Melatonin inhibits oxidative modification of low-density lipoprotein particles in normolipidemic post-menopausal women.
abstract: In this study, we investigated the short-term effect of melatonin on the susceptibility of low-density lipoprotein (LDL) to oxidation in normolipidemic post-menopausal women. Fifteen post-menopausal women received 6.0 mg melatonin daily for 2 wk. Blood samples were obtained before and after the treatment and the plasma levels of total cholesterol, total triglyceride, high-density lipoprotein (HDL)-cholesterol, LDL-cholesterol, LDL-triglyceride, and LDL-apolipoprotein B were determined. LDL oxidation was performed by incubation with copper ions and was analyzed by monitoring the kinetics of conjugated diene formation and measuring the concentration of thiobarbituric-acid-reactive substances (TBARS). LDL-apolipoprotein B derivatization was analyzed by measuring trinitrobenzene sulfonic acid (TNBS) reactivity. Melatonin treatment significantly increased the plasma triglyceride levels (P<0.05), but did not significantly alter the plasma levels of total cholesterol, HDL-cholesterol, or LDL-lipids. The kinetics analysis of conjugated diene production revealed that melatonin treatment significantly prolonged the lag time of conjugated diene formation (from 64.71+/-11.89 to 70.15+/-10.52 min, P<0.05). The oxidation rate and the amount of conjugated diene, however, did not change significantly. The TBARS concentration was significantly reduced by melatonin treatment (from 49.31+/-7.57 to 38.69+/-23.90 nM/mg LDL, P<0.05). Furthermore, melatonin treatment significantly reduced the copper-induced decrease of TNBS reactivity (from 79.43+/-6.19 to 86.50+/-9.07% at 1 hr and from 71.03+/-6.74 to 76.31+/-4.99% at 2 hr, P<0.05). These results indicate that melatonin treatment may reduce LDL susceptibility to oxidative modification in normolipidemic post-menopausal women.
authors.affiliation: Department of Obstetrics and Gynecology, Kochi Medical School, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Wakatsuki
authors.forename: Y
authors.initials: Y
authors.lastname: Okatani
authors.forename: N
authors.initials: N
authors.lastname: Ikenoue
authors.forename: C
authors.initials: C
authors.lastname: Izumiya
authors.forename: C
authors.initials: C
authors.lastname: Kaneda
mesh_terms: D000284:Administration, Oral; D000368:Aged; D001055:Apolipoproteins B / Q000097:blood; D002784:Cholesterol / Q000097:blood; D005260:Female; D016166:Free Radical Scavengers / Q000494:pharmacology*; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood*; D008550:Melatonin / Q000494:pharmacology*; D008875:Middle Aged; D010084:Oxidation-Reduction; D017698:Postmenopause / Q000097:blood*; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D016166:Free Radical Scavengers; D008077:Lipoproteins, LDL; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D002784:Cholesterol; D008550:Melatonin