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过量的膳食组氨酸会降低长 Evans 肉桂大鼠的肝脏铜水平和血清丙氨酸转氨酶活性。

Excess dietary histidine decreases the liver copper level and serum alanine aminotransferase activity in Long-Evans Cinnamon rats.

作者信息

Xu Hong, Sakakibara Shoji, Morifuji Masashi, Salamatulla Quazi, Aoyama Yoritaka

机构信息

Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Sapporo 060-8589, Japan.

出版信息

Br J Nutr. 2003 Sep;90(3):573-9. doi: 10.1079/bjn2003939.

DOI:10.1079/bjn2003939
PMID:13129463
Abstract

Long-Evans Cinnamon (LEC) rats spontaneously develop fulminant hepatitis, associated with excess Cu accumulation in the liver: thus, they are considered an animal model of Wilson's disease. In the present study, we investigated the ability of excess dietary histidine to reduce the excess accumulation of liver Cu in LEC rats by comparing them with Fischer rats. The results clearly showed that the excess-histidine diet markedly stimulated the Cu excretion in urine, and significantly decreased the liver Cu content in LEC rats by 47.5%. The serum Cu content in LEC rats was not influenced by excess dietary histidine. We also compared the effects of excess dietary histidine on some liver antioxidant enzyme activities, liver and serum lipid levels and serum alanine aminotransferase activity of LEC and Fischer rats. Dietary histidine decreased the activities of total and Cu,Zn-superoxide dismutase in the liver of both strains. In LEC rats, the liver cholesterol content decreased, and serum cholesterol and phospholipids levels increased on feeding the excess-histidine diet. When fed on the basal diet, the serum alanine aminotransferase activity was higher in LEC rats than in Fischer rats, but a significant decrease in serum alanine aminotransferase activity of LEC rats was observed on feeding the excess-histidine diet. These results suggest that excess dietary histidine is effective in removing Cu ions from the liver of LEC rats. Thus, it may be of benefit in the prevention or treatment of liver injury in LEC rats and in patients with Wilson's disease.

摘要

长 Evans 肉桂色(LEC)大鼠会自发发展为暴发性肝炎,这与肝脏中铜的过量积累有关:因此,它们被认为是威尔逊病的动物模型。在本研究中,我们通过将 LEC 大鼠与 Fischer 大鼠进行比较,研究了过量膳食组氨酸减少 LEC 大鼠肝脏中过量铜积累的能力。结果清楚地表明,过量组氨酸饮食显著刺激了尿液中的铜排泄,并使 LEC 大鼠的肝脏铜含量显著降低了 47.5%。LEC 大鼠的血清铜含量不受过量膳食组氨酸的影响。我们还比较了过量膳食组氨酸对 LEC 和 Fischer 大鼠的一些肝脏抗氧化酶活性、肝脏和血清脂质水平以及血清丙氨酸转氨酶活性的影响。膳食组氨酸降低了两种品系大鼠肝脏中总超氧化物歧化酶和铜锌超氧化物歧化酶的活性。在 LEC 大鼠中,喂食过量组氨酸饮食时,肝脏胆固醇含量降低,血清胆固醇和磷脂水平升高。当喂食基础饮食时,LEC 大鼠的血清丙氨酸转氨酶活性高于 Fischer 大鼠,但喂食过量组氨酸饮食时,LEC 大鼠的血清丙氨酸转氨酶活性显著降低。这些结果表明,过量膳食组氨酸可有效从 LEC 大鼠肝脏中去除铜离子。因此,它可能对预防或治疗 LEC 大鼠和威尔逊病患者的肝损伤有益。

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Excess dietary histidine decreases the liver copper level and serum alanine aminotransferase activity in Long-Evans Cinnamon rats.过量的膳食组氨酸会降低长 Evans 肉桂大鼠的肝脏铜水平和血清丙氨酸转氨酶活性。
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