N-acetylcysteine stimulates hepatic glycogen deposition in the rat.

A M Itinose, M L Doi-Sakuno, A Bracht
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Abstract

The action of N-acetylcysteine on hepatic glycogen deposition was investigated. Emphasis was also given to the protective action of this compound against hepatic glycogen depletion by paracetamol. Rats fasted for 24 hours were injected intraperitoneally with (1) vehicle, (2) paracetamol (500 mg/kg), (3) N-acetylcysteine (1200 mg/kg) and (4) paracetamol plus N-acetylcysteine. The rats were refed immediately after the drug injections. Paracetamol inhibited glycogen deposition in the 12 hours following injection. The plasma levels of paracetamol were in the range that inhibits energy metabolism in isolated mitochondria and in the isolated perfused liver. N-Acetylcysteine increased the rate of glycogen deposition either in the presence or in the absence of paracetamol. The latter effect may be responsible, partly at least, for the protective action of N-acetylcysteine against glycogen depletion caused by toxic doses of paracetamol.

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n -乙酰半胱氨酸刺激大鼠肝糖原沉积。
研究了n -乙酰半胱氨酸对肝糖原沉积的作用。重点讨论了该化合物对扑热息痛引起的肝糖原耗竭的保护作用。禁食24小时的大鼠腹腔注射(1)载药,(2)扑热息痛(500 mg/kg), (3) n -乙酰半胱氨酸(1200 mg/kg),(4)扑热息痛加n -乙酰半胱氨酸。大鼠在药物注射后立即被喂食。对乙酰氨基酚在注射后12小时内抑制糖原沉积。血浆中扑热息痛的水平在抑制离体线粒体和离体灌注肝的能量代谢的范围内。n -乙酰半胱氨酸在存在或不存在扑热息痛的情况下都增加了糖原沉积的速率。后一种作用可能至少部分地解释了n -乙酰半胱氨酸对有毒剂量扑热息痛引起的糖原耗竭的保护作用。
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