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β-丙氨酸导致的牛磺酸耗竭可抑制用四氯化碳急性处理的小鼠肝毒性的诱导。

Taurine depletion by beta-alanine inhibits induction of hepatotoxicity in mice treated acutely with carbon tetrachloride.

作者信息

Choi Dalwoong, Kim Sun Ju, Kwon Do Young, Lee Sun Young, Kim Young Chul

机构信息

College of Health Science, Korea University, Korea.

出版信息

Adv Exp Med Biol. 2009;643:305-11. doi: 10.1007/978-0-387-75681-3_31.

Abstract

We examined the effect of taurine depletion on hepatic sulfur-containing amino acid metabolism and carbon tetrachloride-induced acute liver injury. Mice were supplemented with beta-alanine (3%) in drinking water for one week. beta-Alanine intake significantly reduced hepatic taurine levels, but did not influence S-adenosylmethionine, S-adenosylhomocysteine, glutathione levels or methionine adenosyltransferase activity in liver. However, hepatic cysteine levels were significantly elevated by beta-alanine administration. Hepatotoxicity caused by carbon tetrachloride (50 microl/kg, ip) in mice fed beta-alanine was decreased, as determined by changes in serum aspartate aminotransferase, alanine aminotransferase and sorbitol dehydrogenase activities. Hepatic glutathione and taurine levels after a carbon tetrachloride challenge were markedly increased by beta-alanine exposure. The results suggest that enhanced availability of cysteine for synthesis of glutathione and/or taurine may account for the hepatoprotective effects of beta-alanine against carbon tetrachloride-induced acute liver injury.

摘要

我们研究了牛磺酸耗竭对肝脏含硫氨基酸代谢及四氯化碳诱导的急性肝损伤的影响。给小鼠饮用含β-丙氨酸(3%)的水一周。摄入β-丙氨酸显著降低了肝脏牛磺酸水平,但对肝脏中S-腺苷甲硫氨酸、S-腺苷高半胱氨酸、谷胱甘肽水平或甲硫氨酸腺苷转移酶活性没有影响。然而,给予β-丙氨酸可使肝脏半胱氨酸水平显著升高。通过血清天冬氨酸氨基转移酶、丙氨酸氨基转移酶和山梨醇脱氢酶活性的变化确定,给予β-丙氨酸的小鼠中四氯化碳(50微升/千克,腹腔注射)引起的肝毒性降低。β-丙氨酸暴露使四氯化碳攻击后的肝脏谷胱甘肽和牛磺酸水平显著升高。结果表明,半胱氨酸用于合成谷胱甘肽和/或牛磺酸的可用性增加可能是β-丙氨酸对四氯化碳诱导的急性肝损伤具有肝保护作用的原因。

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