褪黑素抗自由基作用及其机制

Effect of melatonin on free radicals and its mechanism

目的研究褪黑素（ＭＥＬ）的抗自由基作用，并探讨其作用机制。方法以丙二醛（ＭＤＡ）为指标，考察ＭＥＬ对四氯化碳（ＣＣｌ４）或氰化钾（ＫＣＮ）处理小鼠肝或脑组织脂质的保护作用；考察ＭＥＬ对环磷酰胺所致小鼠骨髓细胞微核的影响；观察ＭＥＬ清除羟自由基（·ＯＨ）作用，及对醋氨酚处理小鼠肝谷胱甘肽（ＧＳＨ）含量和大鼠红细胞超氧化物歧化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）和全血谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的影响。结果ＭＥＬ（２．０，１０．０ｍｇ·ｋｇ－１，ｉｐ）能显著对抗ＣＣｌ４或ＫＣＮ所致小鼠肝脏或脑组织丙二醛含量的增加。ＭＥＬ（１０．０ｍｇ·ｋｇ－１，ｉｐ）可明显抑制环磷酰胺引起的小鼠骨髓细胞微核增多。ＭＥＬ（０．０７８～５．０ｍｍｏｌ·Ｌ－１）可直接清除·ＯＨ。ＭＥＬ（１．０，１０．０ｍｇ·ｋｇ－１，ｉｐ）可显著对抗醋氨酚（ＡＡＰ）所致小鼠ＧＳＨ的耗竭作用。ＭＥＬ（１．０，５．０ｍｇ·ｋｇ－１，ｉｐ）亦可显著提高大鼠红细胞内ＳＯＤ、ＣＡＴ、全血ＧＳＨ－Ｐｘ活性。结论ＭＥＬ可保护脂质和核酸免受过氧化损伤，这可能与其直接清除·ＯＨ，提高机体ＧＳＨ含量及增强ＳＯＤ、ＣＡＴ、ＧＳＨ－Ｐｘ活力有关。

AIM To investigate the role and mechanism of melatonin (MEL) on anti free radicals. METHODS The MDA content was measured in liver or brain tissues in mice which were pretreated by CCl 4 or KCN in vivo. The micronuclei induced by cyclophosphamide (CY) were examined. The role of MEL in scavenging ·OH, countering the exhausting GSH induced by acetaminophen (AAP) in mice and enhancing erythrocyte superoxide dismutase (SOD), catalase (CAT) and whole blood glutothine peroxidase (GSH Px) in rats were also investigated. RESULTS MEL (2 0,10 0 mg·kg -1 ,ip) had a great reducing effect on MDA induced by CCl 4 or KCN in liver or brain tissues respectively. MEL(10 0 mg·kg -1 ,ip) conld also inhibit the increasing micronuclei induced by CY. MEL(0 078￣5 0 mmol·L -1 ) could scavenge ·OH directly. MEL (1 0, 10 0 mg·kg -1 ,ip) significantly counteracted the exhausting GSH induced by AAP in mice liver tissus. MEL(1 0, 5 0 mg·kg -1 ,ip) also had a potentiating enhancement on activities of erythrocyte SOD, CAT and whole blood GSH Px in rats. CONCLUSION MEL could protect lipid and nuclei acid against free radical damage, which may be due to the action of MEL in scavenging ·OH, increasing GSH content and activity of SOD, CAT and GSH Px.