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Protective Effect of Melatonin Against Mitomycin C-Induced Genotoxic Damage in Peripheral Blood of Rats

机译:褪黑素对丝裂霉素C致大鼠外周血遗传毒性损伤的保护作用

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摘要

Mitomycin C (MMC) generates free radicals when metabolized. We investigated the effect of melatonin against MMC-induced genotoxicity in polychromatic erythrocytes and MMC-induced lipid peroxidation in brain and liver homogenates. Rats (N = 36) were classified into 4 groups: control, melatonin, MMC, and MMC + melatonin. Melatonin and MMC doses of 10 mg/kg and 2 mg/kg, respectively, were injected intraperitoneally. Peripheral blood samples were collected at 0, 24, 48, 72, and 96 hours posttreatment and homogenates were obtained at 96 hours posttreatment. The number of micronucleated polychromatic erythrocytes (MN-PCE) per 1000 PCE was used as a genotoxic marker. Malondialdehyde (MDA) plus 4-hydroxyalkenal (4-HDA) levels were used as an index of lipid peroxidation. The MMC group showed a significant increase in MN-PCE at 24, 48, 72, and 96 hours that was significantly reduced with melatonin begin coadministrated. No significant differences were found in lipid peroxidation. Our results indicate that MMC-induced genotoxicity can be reduced by melatonin.
机译:丝裂霉素C(MMC)代谢时会产生自由基。我们调查了褪黑素对MMC诱导的多色红细胞遗传毒性和MMC诱导的脑和肝匀浆脂质过氧化的影响。将大鼠(N = 36)分为4组:对照组,褪黑激素,MMC和MMC +褪黑激素。腹膜内注射褪黑激素和MMC剂量分别为10 mg / kg和2 mg / kg。在处理后0、24、48、72和96小时收集外周血样品,并在处理后96小时获得匀浆。每1000 PCE中微核多色红细胞(MN-PCE)的数量用作遗传毒性标记。丙二醛(MDA)和4-羟基烯醛(4-HDA)的水平用作脂质过氧化的指标。 MMC组在24、48、72和96小时显示MN-PCE显着增加,而开始同时服用褪黑激素则明显减少。脂质过氧化没有发现显着差异。我们的结果表明,褪黑激素可以降低MMC诱导的遗传毒性。

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