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Melatonin inhibits oxidative modification of low‐density lipoprotein particles in normolipidemic post‐menopausal women
Author(s) -
Wakatsuki Akihiko,
Okatani Yuji,
Ikenoue Nobuo,
Izumiya Chiaki,
Kaneda Chitose
Publication year - 2000
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1034/j.1600-079x.2001.280302.x
Subject(s) - melatonin , tbars , medicine , chemistry , endocrinology , triglyceride , low density lipoprotein , apolipoprotein b , lipoprotein , cholesterol , high density lipoprotein , lipid peroxidation , biochemistry , oxidative stress
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.