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目的 探讨褪黑素对四氯化碳肝毒性的保护作用。方法 给予小鼠四氯化碳（５ ｍｌ·ｋｇ － １ ） ，继后每隔６ ｈ ｉｐ 褪黑素１０ ｍ ｇ·ｋｇ － １ 。用胶原酶消化法分离小鼠肝细胞后，依次加用褪黑素（１０ － ５ ～１０ － １ １ ｍｏｌ· Ｌ－ １ ） 和四氯化碳（２０ ｍ ｍ ｏｌ· Ｌ－ １ ） 。以测定丙氨酸氨基转换酶（ Ａ Ｌ Ｔ） ，丙二醛（ Ｍ Ｄ Ａ） 和谷胱甘肽过氧化物酶活力，作为四氯化碳肝损伤的指标。用 Ｍ Ｔ Ｔ 法检测肝细胞活力。结果 四氯化碳可使小鼠血液 Ａ Ｌ Ｔ 活性和肝 Ｍ Ｄ Ａ 含量明显上升。体内应用 Ｍ Ｔ １０ ｍ ｇ·ｋｇ － １ ，则明显降低肝匀浆 Ｍ Ｄ Ａ 含量（ Ｐ＜ ００１） ， 对血浆 Ａ Ｌ Ｔ 活性无明显影响。体外应用 Ｍ Ｔ（１０ － ５ ～１０ － ７ ｍｏｌ· Ｌ－ １ ） 亦可使肝细胞 Ｍ Ｄ Ａ 含量下降（ Ｐ＜ ００５） ，同时还可使肝细胞 Ａ Ｌ Ｔ 释放率下降，细胞活力上升（ Ｐ＜ ００５） 。结论 Ｍ Ｔ 拮抗 Ｃ Ｃｌ４ 肝毒性的作用可能与其抗氧化能力有关
Objective To investigate the protective effect of melatonin on hepatotoxicity of carbon tetrachloride. Methods Mice were given carbon tetrachloride (5 ml · kg - 1), followed by ip melatonin at 10 m g · kg - 1 every 6 h. After the mouse hepatocytes were isolated by collagenase digestion, melatonin (10-5-10-1 mol · L -1) and carbon tetrachloride (20 mg · L -1) were added sequentially. Alanine aminotransferase (ALT), malondialdehyde (MDA) and glutathione peroxidase activity were measured as indicators of carbon tetrachloride-induced liver injury. Liver cell viability was measured by MTT method. Results Carbon tetrachloride significantly increased blood ALT activity and liver MDA content in mice. In vivo application of MT 10 m g · kg - 1 significantly decreased the content of M D A in the liver homogenate (P <001), but had no significant effect on the activity of A L T in plasma. In vitro application of M T (10 -5 to 10 -7 mol · L -1) also decreased the content of M D A in hepatocytes (P <005), and at the same time decreased the release of A L T from hepatocytes. Vitality increased (P <005). Conclusion The antagonistic effect of M T on CCl4 hepatotoxicity may be related to its antioxidant capacity