Protective effect of melatonin against nodularin-induced oxidative stress in mouse liver
Protective effect of melatonin against nodularin-induced oxidative stress in mouse liver
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DOI：
10.1007/s00204-001-0310-x
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发表时间：
2002-04-01
影响因子：
6.1
通讯作者：
Nowak, M
中科院分区：
文献类型：
--
作者：
Lankoff, A;Banasik, A;Nowak, M
结节素是一种来自蓝藻菌的肝毒素，可抑制蛋白磷酸酶1和2，并具有促肿瘤活性。本文旨在探讨结核素是否能诱导小鼠肝组织氧化应激，以及褪黑素（抗氧化损伤的保护性化合物）是否能抑制结核素的活性。本实验研究了结节素（1、5、10 mg/kg体重）和褪黑素（5、10、15 mg/kg体重）对小鼠肝脏超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSH-Px）活性的影响。每7天向小鼠腹腔注射结节素可使所有估计酶的活性呈剂量依赖性降低。每7天向动物腹腔注射褪黑素可增加SOD、CAT和GSH-Px的活性，且这种作用呈浓度依赖性。与结核素组相比，共处理（结核素5杯/kg体重+褪黑素5、10和15 mg/kg体重/ 7天）和后处理褪黑素（结核素5杯/kg体重/ 7天+褪黑素5、10和15 mg/kg体重/ 7天）增加了SOD、CAT和GSH-Px的活性。经褪黑素预处理后，该组与结节素组无显著差异。综上所述，这些发现提示结核素的毒性可能涉及氧化损伤。此外，与10和15 mg/kg体重的褪黑素共处理和后处理可防止结节素诱导的氧化应激。褪黑素预处理无保护作用。
Nodularin is a hepatotoxin from a cyanobacterium, Nodularia spumigena, that inhibits protein phosphatases 1 and 2 and posseses tumor-promoting activity. The aim of this paper was to examine whether nodularin is able to induce oxidative stress in mouse liver tissue and whether melatonin (protective compound against oxidative damage) could supress the activity of nodularin. We studied the effect of nodularin (1, 5, and 10 mug/kg body weight) and melatonin (5, 10, and 15 mg/kg body weight) administration on the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in mouse liver. Intraperitoneal treatment of mice with nodularin per 7 days decreased the activities of all estimated enzymes in a dose-dependent manner. Intraperitoneal treatment of animals with melatonin per 7 days increased the activities of SOD, CAT, and GSH-Px and this effect was concentration-dependent. Co-treatment (nodularin 5 mug/kg body weight + melatonin 5, 10, and 15 mg/kg body weight per 7 days) and post-treatment with melatonin (nodularin 5 mug/kg body weight per 7 days + melatonin 5, 10, and 15 mg/kg body weight per next 7 days) increased the activities of SOD, CAT, and GSH-Px in comparison to the nodularin group. No significant differences from the nodularin group were noted in the group after pre-treatment with melatonin. In conclusion, these findings suggest that oxidative damage may be involved in the toxicity of nodularin. Moreover, co-treatment and post-treatment with 10 and 15 mg/kg body weight of melatonin may protect against nodularin-induced oxidative stress. There was no protective effect of pre-treatment with melatonin.