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Compound 48/80, a Mast Cell Degranulator, Induces Oxidative Stress in Rat Livers

机译:化合物48/80,桅杆细胞脱杆剂,诱导大鼠肝脏氧化应激

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We examined whether compound 48/80 (C48/80), a mast cell degranulator, induces oxidative stress in rat livers. Fasted male Wistar rats were injected with C48/80 (0.75 mg/kg, i.p), Increases in hepatic lipid peroxide, total ascorbic acid (AA), reduced AA, and oxidized AA levels and a decrease in hepatic reduced glutathione level occurred 3 h after C48/80 treatment. Hepatic gly-cogen level decreased 3 and 6 h after C48/80 treatment, Hepatic vitamin E level was not changed by C48/80 treatment. When vitamin E (200 mg/kg) was orally administered to C48/80-treated rats at 0,5 h after the treatment, all these changes found at 3 h after the treatment were almost completely attenuated. These results indicate that C48/80 induces oxidative stress in rat livers through an increase in hepatic AA synthesis associated with glutathione depletion.
机译:我们检查了化合物48/80(C48 / 80),桅杆细胞脱液剂,诱导大鼠肝脏氧化应激。用C48 / 80(0.75mg / kg,IP)注射仓位的雄性Wistar大鼠,增加肝脂过氧化物,总抗坏血酸(AA),降低AA,并氧化AA水平和肝脏降低的谷胱甘肽水平发生了3小时C48 / 80治疗后。 C48 / 80治疗后,肝脏甘露胆汁水平降低3和6小时,C48 / 80治疗不改变肝维生素E水平。当治疗后0.5小时的维生素E(200mg / kg)口服给予C48 / 80-处理的大鼠时,治疗后3小时发现所有这些变化几乎完全衰减。这些结果表明C48 / 80通过与谷胱甘肽耗竭相关的肝脏AA合成的增加,C48 / 80诱导大鼠肝脏的氧化应激。

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